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Hypermethylation of Mest promoter causes aberrant Wnt signaling in patients with Alzheimer's disease

Hypermethylation of Mest promoter causes aberrant Wnt signaling in patients with Alzheimer’s disease

Alzheimer’s illness (AD) is a progressive neurodegenerative dysfunction that results in dementia and behavioral adjustments. Extracellular deposition of amyloid plaques (Aβ) and intracellular deposition of neurofibrillary tangles in neurons are the foremost pathogenicities of AD.
Nevertheless, medicine concentrating on these therapeutic targets should not efficient. Subsequently, novel targets for the remedy of AD urgently should be recognized. Expression of the mesoderm-specific transcript (Mest) is regulated by genomic imprinting, the place solely the paternal allele is lively for transcription.
We recognized hypermethylation on the Mest promoter, which led to a discount in Mest mRNA ranges and activation of Wnt signaling in mind tissues of AD sufferers. Mest knockout (KO) utilizing the CRIPSR/Cas9 system in mouse embryonic stem cells and P19 embryonic carcinoma cells results in neuronal differentiation arrest.
Depletion of Mest in major hippocampal neurons by way of lentivirus expressing shMest or inducible KO system causes neurodegeneration. Notably, depletion of Mest in major cortical neurons of rats results in tau phosphorylation on the S199 and T231 websites.
General, our knowledge recommend that hypermethylation of the Mest promoter could trigger or facilitate the development of AD.

Environment friendly Era of Multi-gene Knockout Cell Strains and Affected person-derived Xenografts Utilizing Multi-colored Lenti-CRISPR-Cas9

CRISPR-Cas9 based mostly knockout methods are more and more used to investigate gene perform. Nevertheless, redundancies and overlapping capabilities in organic signaling pathways can name for producing multi-gene knockout cells, which stays a comparatively laborious course of.
Right here we element the applying of multi-color LentiCRISPR vectors to concurrently generate single and a number of knockouts in human cells. We offer an entire protocol, together with information RNA design, LentiCRISPR cloning, viral manufacturing and transduction, in addition to methods for sorting and screening knockout cells.
The validity of the method is demonstrated by the simultaneous deletion of as much as 4 programmed cell dying mediators in leukemic cell strains and patient-derived acute lymphoblastic leukemia xenografts, during which single cell cloning will not be possible.
This protocol permits any lab with entry to primary mobile biology tools, a biosafety stage 2 facility and fluorescence-activated cell sorting capabilities to generate single and multi-gene knockout cell strains or major cells effectively inside one month.

In vivo supply of CRISPR-Cas9 therapeutics: Progress and challenges

Inside lower than a decade since its inception, CRISPR-Cas9-based genome enhancing has been quickly superior to human scientific trials in a number of illness areas.
Though it’s extremely anticipated that this revolutionary expertise will carry novel therapeutic modalities to many ailments by exactly manipulating mobile DNA sequences, the low effectivity of in vivo supply have to be enhanced earlier than its therapeutic potential might be absolutely realized.
Right here we talk about the latest progress of in vivo supply of CRISPR-Cas9 programs, spotlight progressive viral and non-viral supply applied sciences, emphasize excellent supply challenges, and supply probably the most up to date views.

DNA damage-inducible transcript Three restrains osteoclast differentiation and performance

DNA damage-inducible transcript 3 (DDIT3), a member of the CCAAT/enhancer-binding protein (C/EBP) household, is concerned in mobile apoptosis and differentiation. DDIT3 participates within the regulation of adipogenesis and osteogenesis in vitro and in vivo.
Nevertheless, the position of DDIT3 in osteoclastogenesis will not be but identified. On this examine, the involvement of DDIT3 in osteoclast differentiation and performance was reported for the primary time. CRISPR/Cas9-mediated DDIT3 knockout (KO) mice had been generated for practical evaluation.
Tartrate-resistant acid phosphatase (TRAP) staining of distal femurs confirmed elevated optimistic cells in DDIT3 KO mice. DDIT3 expression was downregulated in the course of the receptor activator of nuclear issue κB ligand (RANKL)-induced osteoclast differentiation of bone marrow-derived macrophages (BMMs).
The lack of DDIT3 elevated the expression of osteoclast-specific markers, together with nuclear issue of activated T-cells cytoplasmic 1 (NFATc1), TRAP, cathepsin Ok (CTSK), and dendritic cell-specific transmembrane protein (DC-STAMP) and promoted the formation of TRAP-positive multinucleated osteoclasts.
The actin ring quantity and resorption space of bone slices had been additionally elevated in DDIT3 KO BMMs. Lentivirus-mediated DDIT3 overexpression considerably inhibited the osteoclast differentiation of RAW264.7 cells.
Within the tumor necrosis factor-α-induced osteolysis mannequin, DDIT3 deficiency enhanced osteoclast formation and aggravated bone resorption. DDIT3 inhibited osteoclast differentiation by regulating the C/EBPα-CTSK axis.
Moreover, DDIT3 KO intensified the RANKL-triggered activation of the MAPKs and Akt signaling pathways. Taken collectively, the outcomes revealed the important position of DDIT3 in osteoclastogenesis in vitro and in vivo and its shut relationship with osteoclast-associated transcription components and pathways.

SREBP1 website 1 protease inhibitor PF-429242 suppresses renal cell carcinoma cell progress

Renal cell carcinoma (RCC) cells have elevated lipogenesis and ldl cholesterol synthesis. Sterol regulatory element-binding protein-1 (SREBP1) is cleaved by website 1 protease (S1P) to launch the transcriptionally lively amino-terminal area.
PF-429242 is a potent and aggressive S1P inhibitor. We right here examined its exercise in RCC cells. In established and first human RCC cells, PF-429242 potently inhibited cell proliferation, migration, and invasion. The S1P inhibitor provoked apoptosis activation in RCC cells.
Moreover, shRNA-mediated S1P silencing or CRISPR/Cas9-induced S1P knockout led to RCC cell progress inhibition and apoptosis activation. Conversely, ectopic overexpression of SREBP1 or S1P augmented RCC cell proliferation and migration.
Each day i.v. injection of a single dose of PF-429242 robustly inhibited RCC xenograft progress in extreme mixed immunodeficiency mice. Moreover, intratumoral injection of S1P shRNA lentivirus inhibited RCC xenograft progress in mice.
SREBP1, S1P, and its goal gene low density lipoprotein receptor (LDLR) had been considerably elevated in human RCC tissues. These outcomes recommend that concentrating on S1P by PF-429242 inhibited RCC cell progress in vitro and in vivo.

Novel vectors and approaches for gene remedy in liver ailments

Gene remedy is changing into an more and more priceless instrument to deal with many genetic ailments with no or restricted remedy choices. That is the case for a whole lot of monogenic metabolic problems of hepatic origin, for which liver transplantation stays the one treatment.
Moreover, the liver incorporates 10-15% of the physique’s whole blood quantity, making it excellent to be used as a manufacturing facility to secrete proteins into the circulation. In current a long time, an increasing toolbox has turn out to be out there for liver-directed gene supply.
Though viral vectors have lengthy been the popular strategy to focus on hepatocytes, an growing variety of non-viral vectors are rising as extremely environment friendly autos for the supply of genetic materials.
Herein, we evaluation advances in gene supply vectors concentrating on the liver and extra particularly hepatocytes, masking methods based mostly on gene addition and gene enhancing, in addition to the thrilling outcomes obtained with using RNA as a therapeutic molecule.

CD47 CRISPR/Cas9 Lentivirus (Integrating)

78056 500 µl x 2
EUR 795
Description: CD47 (also known as Rh-associated protein, GP42, Integrin-Associated Protein (IAP), or Neurophilin) is an immunoglobulin-like protein that interacts with its receptor, Signal-regulatory protein alpha (SIRPα), on macrophages. This binding interaction regulates transmigration, oxidative burst cytokine production, and phagocytosis, generating a "don't eat me" signal. CD47 is ubiquitously expressed on the surface of normal cells, but is overexpressed in numerous cancer cells where it is thought to contribute to the resistance of tumors to phagocyte-dependent clearance._x000D_The CD47 CRISPR Lentiviruses are replication incompetent, HIV-based VSV-G pseudo-typed lentiviral particles that are ready to be transduced into almost all types of mammalian cells, including primary and non-dividing cells. The particles contain a CRISPR/Cas9 gene driven by an EF1a promoter, along with 4 sgRNA (single guide RNA) targeting human CD47 (NM_198793.2) driven by a U6 promoter (Figures 1 and 2)._x000D_The integrating lentivirus integrates randomly into the cell's genome to express both the Cas9 and sgRNA. Puromycin selection increases the knockout efficiency by forcing high expression levels of both Cas9 and the sgRNA, and can be used with the integrating lentivirus to quickly and easily achieve high knockdown efficiencies in a cell pool. Efficiencies also depend on the cell type and the gene of interest._x000D_

CRBN CRISPR/Cas9 Lentivirus (Integrating)

78517 500 µl x 2
EUR 795
Description: Cereblon (CRBN) forms an E3 ubiquitin ligase complex which is responsible for ubiquitinating proteins that regulate various developmental processes. CRBN also binds to Calcium Activated Potassium Channel subunit alpha-1 (KCNMA1) to regulate ion transport. Moreover, mutations in CRBN may play an underlying role in tumor cells acquiring resistance to immunotherapy.The CRBN CRISPR/Cas9 Lentiviruses are replication incompetent, HIV-based VSV-G pseudotyped lentiviral particles that are ready to transduce almost all types of mammalian cells, including primary and non-dividing cells. The particles contain a CRISPR/Cas9 gene driven by an EF1a promoter, along with 5 sgRNA (single guide RNA) targeting human CRBN.The DNA transduced by this lentivirus integrates randomly into the cellular genome to express both Cas9 and sgRNA. Puromycin selection increases the knockout efficiency by forcing high expression levels of both Cas9 and the sgRNA, and can be used with the integrating lentivirus to quickly and easily achieve high knockdown efficiencies in a cell pool. Efficiencies also depend on the cell type.

CTLA4 CRISPR/Cas9 Lentivirus (Integrating)

78054 500 µl x 2
EUR 795
Description: CTLA4 (Cytotoxic T-Lymphocyte Associated Protein), also known as CD152, is a protein receptor that functions as an immune checkpoint. It is expressed by activated T-cells and transmits an inhibitory signal to T-cells. CTLA4 is homologous to the T-cell co-stimulatory protein CD28, and both molecules bind to CD80 (B7-1) and CD86 (B7-2) on antigen-presenting cells. CTLA4 binds CD80 and CD86 with greater affinity and avidity than CD28, thus enabling it to out-compete CD28 for its ligands and act as an "off" switch when bound to CD80 or CD86. CTLA4 is an important immunotherapy target for the treatment of cancer and autoimmune diseases._x000D_
The CTLA4 CRISPR Lentiviruses are replication incompetent, HIV-based VSV-G pseudo-typed lentiviral particles that are ready to be transduced into almost all types of mammalian cells, including primary and non-dividing cells. The particles contain a CRISPR/Cas9 gene driven by an EF1a promoter, along with 4 sgRNA (single guide RNA) targeting human CTLA4, GenBank Accession #NM_005214, driven by a U6 promoter (Figures 1 and 2)._x000D_The integrating lentivirus integrates randomly into the cell's genome to express both the Cas9 and sgRNA. Puromycin selection increases the knockout efficiency by forcing high expression levels of both Cas9 and the sgRNA, and can be used with the integrating lentivirus to quickly and easily achieve high knockdown efficiencies in a cell pool. Efficiencies also depend on the cell type and the gene of interest._x000D_

TIGIT CRISPR/Cas9 Lentivirus (Integrating)

78058 500 µl x 2
EUR 795
Description: TIGIT (T-cell immunoreceptor with Ig and ITIM domains; VSTM3; VSIG9) is a co-inhibitory receptor that is highly expressed in Natural Killer (NK) cells and activated CD4+, CD8+, and regulatory T-cells. Interaction with the Poliovirus Receptor (PVR; CD155) on antigen presenting cells, such as dendritic cells, recruits either the Src homology (SH) domain-containing tyrosine phosphatases SHP1 and SHP2, or the Inositol phosphatase SHIP1 and SHIP2, to the TIGIT ITIM domain. This increases IL-10 release and suppresses NF-κB and NFAT T-cell receptor (TCR) signaling, which blocks T-cell proliferation and cytokine production. TIGIT also serves as a competitive inhibitor of CD226, a costimulatory receptor for CD155. TIGIT-targeting antibodies which block this T-cell intrinsic inhibitory effect have shown enhanced anti-tumor and anti-viral functions in preclinical studies._x000D_
The TIGIT CRISPR Lentiviruses are replication incompetent, HIV-based VSV-G pseudo-typed lentiviral particles that are ready to be transduced into almost all types of mammalian cells, including primary and non-dividing cells. The particles contain a CRISPR/Cas9 gene driven by an EF1a promoter, along with 4 sgRNA (single guide RNA) targeting human TIGIT (GenBank Accession #NM_173799) driven by a U6 promoter._x000D_
The integrating lentivirus integrates randomly into the cell's genome to express both the Cas9 and sgRNA. Puromycin selection increases the knockout efficiency by forcing high expression levels of both Cas9 and the sgRNA, and can be used with the integrating lentivirus to quickly and easily achieve high knockdown efficiencies in a cell pool. Efficiencies also depend on the cell type and the gene of interest.

NLRP3 CRISPR/Cas9 Lentivirus (Integrating)

78545 500 µl x 2
EUR 995
Description: NLR family Pyrin domain containing 3 (NLRP3) is expressed in macrophages and is a component of inflammasomes. NLRP3 detects uric acid and extracellular ATP in damaged tissue and interacts with a pro-apoptotic protein that recruits caspases. This complex is also an upstream activator of NF-κB signaling and triggers an immune response as part of the innate immune system. Mutations in NLRP3 are known to cause autoinflammatory and neuroinflammatory diseases, such as Alzheimer's, Parkinson's, and prion disease. The NLRP3 CRISPR/Cas9 Lentiviruses are replication incompetent, HIV-based VSV-G pseudo-typed lentiviral particles ready to infect most types of mammalian cells, including primary and non-dividing cells. The particles contain a CRISPR/Cas9 gene driven by an EF1a promoter, along with 5 sgRNA (single guide RNA) targeting human NLRP3 (Figure 1 and Table 1), allowing the knockdown of NLRP3 in transduced cells.The DNA transduced by the integrating lentivirus integrates randomly into the cellular genome to express both Cas9 and sgRNA. Puromycin selection increases the knockout efficiency by forcing high expression levels of both Cas9 and the sgRNA, and can be used with the integrating lentivirus to quickly and easily achieve high knockdown efficiencies in a cell pool. Knockdown efficiencies also depend on the cell type.

FCGR2A CRISPR/Cas9 Lentivirus (Integrating)

78537 500 µl x 2
EUR 795
Description: Fc Gamma Receptor 2A (also known as CD32A, Fc-gamma-RIIa, FcgRIIa) is a low affinity Fc receptor for immunoglobulin G, encoded by the FCGR2A gene. Fc Gamma Receptor 2A is a cell surface receptor that is expressed on a variety of immune cells such as macrophages and neutrophils. It is involved in phagocytosis and in the clearing of spent immune complexes from the circulation. A polymorphism in FCGR2A has been associated with increased risks of nephritis and lupus.The FCGR2A CRISPR/Cas9 Lentiviruses are replication incompetent, HIV-based VSV-G pseudo-typed lentiviral particles that are ready to transduce into almost all types of mammalian cells, including primary and non-dividing cells. The particles contain a CRISPR/Cas9 gene driven by an EF1a promoter, along with 5 sgRNA (single guide RNA) targeting human FCGR2A.

PD-1 CRISPR/Cas9 Lentivirus (Integrating)

78052 500 µl x 2
EUR 820
Description: The binding of Programmed Cell Death Protein 1 (PD-1), a receptor expressed on activated T-cells, to its ligands, PD-L1 and PD-L2, negatively regulates immune responses. PD-1 ligands are found on most cancers, and the PD-1:PD-L1/2 interaction inhibits T-cell activity and enables cancer cells to escape immune surveillance. The PD-1:PD-L1/2 pathway is also involved in regulating autoimmune responses, making these proteins promising therapeutic targets for a number of cancers, as well as multiple sclerosis, arthritis, lupus, and type I diabetes._x000D_
The PD-1 CRISPR Lentiviruses are replication incompetent, HIV-based VSV-G pseudo-typed lentiviral particles that are ready to be transduced into almost all types of mammalian cells, including primary and non-dividing cells. The particles contain a CRISPR/Cas9 gene driven by an EF1a promoter, along with 4 sgRNA (single guide RNA) targeting human PD-1 (Programmed Cell Death 1, PDCD1, CD279, GenBank Accession #NM_005018) driven by a U6 promoter (Figures 1 and 2)._x000D_
The integrating lentivirus integrates randomly into the cell's genome to express both the Cas9 and sgRNA. Puromycin selection increases the knockout efficiency by forcing high expression levels of both Cas9 and the sgRNA, and can be used with the integrating lentivirus to quickly and easily achieve high knockdown efficiencies in a cell pool. Efficiencies also depend on the cell type and the gene of interest._x000D_ _x000D_

PD-L1 CRISPR/Cas9 Lentivirus (Integrating)

78057 500 µl x 2
EUR 795
Description: The binding of Programmed Cell Death Protein 1 (PD-1), a receptor expressed on activated T-cells, to its ligands, PD-L1 and PD-L2, negatively regulates immune responses. The PD-1 ligands are found on most cancers, and the PD-1:PD-L1/2 interaction inhibits T-cell activity and allows cancer cells to escape immune surveillance. The PD-1:PD-L1/2 pathway is also involved in regulating autoimmune responses, making these proteins promising therapeutic targets for a number of cancers, as well as multiple sclerosis, arthritis, lupus, and type I diabetes._x000D_The PD-L1 CRISPR Lentiviruses are replication incompetent, HIV-based, VSV-G pseudo-typed lentiviral particles that are ready to be transduced into almost all types of mammalian cells, including primary and non-dividing cells. The particles contain a CRISPR/Cas9 gene driven by an EF1a promoter, along with 4 sgRNA (single guide RNA) targeting human PD-L1 (Programmed Cell Death 1 Ligand 1, CD274, B7 homolog 1 (B7-H1), GenBank accession #NM_021893) driven by a U6 promoter (Figures 1 and 2)._x000D_The integrating lentivirus integrates randomly into the cell's genome to express both the Cas9 and sgRNA. Puromycin selection increases the knockout efficiency by forcing high expression levels of both Cas9 and the sgRNA, and can be used with the integrating lentivirus to quickly and easily achieve high knockdown efficiencies in a cell pool. Efficiencies also depend on the cell type and the gene of interest._x000D_

TCR CRISPR/Cas9 Lentivirus (Non-Integrating)

78062 500 µl x 2
EUR 995
Description: The T-Cell Receptor (TCR) is found on the surface of T-cells and is responsible for recognizing antigens bound to MHC (Major Histocompatibility Complex) molecules. Activation of the TCR results in activation of downstream NFAT signaling. The TCR consists of a heterodimer of two different protein chains, of which the alpha (α) and beta (β) chains are the predominant chains._x000D_
The TCR CRISPR Lentiviruses are replication incompetent, HIV-based VSV-G pseudo-typed lentiviral particles that are ready to be transduced into almost all types of mammalian cells, including primary and non-dividing cells. The particles contain a CRISPR/Cas9 gene driven by an EF1a promoter, along with 4 sgRNA (single guide RNA) targeting human TRAC (T-Cell Receptor Alpha Constant) and human TRBC1 (T-Cell Receptor Beta Constant 1) regions of the α and β chains._x000D_
The non-integrating lentivirus is made with a mutated integrase, resulting in only transient expression of the Cas9 and sgRNA. Although using the non-integrating lentivirus results in lower knockdown efficiency, the Cas9 isn't permanently expressed, which lowers the risk of off-targeting, and there are no random integrations into the cell's genome. Knockout cell lines can still be generated following cell sorting or limited dilution, because even though the Cas9 and sgRNA expression is transient, the changes in the genomic DNA from the Cas9 nuclease activity and NHEJ repair are permanent._x000D_

CD5 (Human) CRISPR/Cas9 Lentivirus (Integrating)

78119 500 µl x 2
EUR 795
Description: The CD5 CRISPR Lentiviruses are replication incompetent, HIV-based VSV-G  pseudotyped lentiviral particles that are ready to  infect almost all types of mammalian cells, including primary and non-dividing cells. The particles contain a CRISPR/Cas9 gene driven by an EF1a promoter, along with 5 sgRNA (single guide RNA) targeting human CD5 driven by a U6 promoter.The integrating lentivirus integrates randomly into the  cellular genome to express both Cas9 and the sgRNA. Puromycin selection forces high expression levels of both Cas9 and the sgRNA, and can be used with the integrating lentivirus to quickly and easily achieve high knockdown efficiencies in a cell pool. Efficiencies may vary, depending on the cell type and the gene of interest.

B2M (Human) CRISPR/Cas9 Lentivirus (Integrating)

78340 500 µl x 2
EUR 795
Description: Beta-2 Microglobulin (B2M) is a required component of Major Histocompatibility Complex (MHC) class 1 molecules, which present peptide fragments from within the cell to cytotoxic T-cells as part of the adaptive immune system. The B2M CRISPR/Cas9 Lentiviruses are replication incompetent, HIV-based, VSV-G pseudotyped lentiviral particles that are ready to infect almost all types of mammalian cells, including primary and non-dividing cells. The particles contain a CRISPR/Cas9 gene driven by an EF1a promoter, along with 5 sgRNA (single guide RNAs) targeting human B2M driven by a U6 promoter.The integrating lentivirus integrates randomly into the cellular genome to express both Cas9 and the sgRNA. Puromycin selection forces high expression levels of both Cas9 and the sgRNA, and can be used with the integrating lentivirus to quickly and easily achieve high knockdown efficiencies in a cell pool. Efficiencies will depend on the cell type and the gene of interest.

LAG3 CRISPR/Cas9 Lentivirus (Non-Integrating)

78060 500 µl x 2
EUR 995
Description: Lymphocyte-activation gene 3 (LAG3, CD223) is a cell surface protein that belongs to the immunoglobulin (Ig) superfamily. LAG3 is expressed on activated T-cells, Natural Killer cells, B-cells, and plasmacytoid dendritic cells. Its main ligand is the MHC class II, to which it binds with higher affinity than CD4. It negatively regulates cellular proliferation, activation, and homeostasis of T-cells in a similar fashion as CTLA-4 and PD-1, and has been reported to play a role in T-reg suppressive function. A number of LAG3 antibodies are in preclinical development for the treatment of cancer and autoimmune disorders. LAG3 may be a better immune checkpoint inhibitor target than CTLA-4 or PD-1, because antibodies targeting CTLA-4 or PD-1 only activate effector T-cells while failing to inhibit T-reg activity, whereas an antagonist LAG3 antibody can both activate effector T-cells (by downregulating the LAG3 inhibiting signal) and inhibit induced (i.e. antigen-specific) T-reg suppressive activity.

The LAG3 CRISPR Lentiviruses are replication incompetent, HIV-based, VSV-G pseudo-typed lentiviral particles that are ready to be transduced into almost all types of mammalian cells, including primary and non-dividing cells. The particles contain a CRISPR/Cas9 gene driven by an EF1a promoter, along with 4 sgRNA (single guide RNA) targeting human LAG3 (GenBank Accession #NM_002286) driven by a U6 promoter._x000D_Note: unlike Human LAG3 CRISPR/Cas9 Lentivirus (Integrating) (BPS Bioscience, #78053), the Human LAG3 CRISPR/Cas9 Lentivirus (Non-Integrating) is made with a mutated Integrase, resulting in only transient expression of the Cas9 and LAG3-targeting sgRNA. While this may minimize potential off-targeting risks due to either prolonged expression or integration of the Cas9, puromycin selection should not be used for more than 48 hours post-transduction, which may lower knockout efficiency.

CD47 CRISPR/Cas9 Lentivirus (Non-Integrating)

78063 500 µl x 2
EUR 995
Description: CD47 (also known as Rh-associated protein, GP42, Integrin-Associated Protein (IAP), or Neurophilin) is an immunoglobulin-like protein that interacts with its receptor, Signal-regulatory protein alpha (SIRPα), on macrophages. This binding interaction regulates transmigration, oxidative burst cytokine production, and phagocytosis, generating a "don't eat me"signal. CD47 is ubiquitously expressed on the surface of normal cells, but is overexpressed in numerous cancer cells where it is thought to contribute to the resistance of tumors to phagocyte-dependent clearance._x000D_The CD47 CRISPR Lentiviruses are replication incompetent, HIV-based VSV-G pseudo-typed lentiviral particles that are ready to be transduced into almost all types of mammalian cells, including primary and non-dividing cells. The particles contain a CRISPR/Cas9 gene driven by an EF1a promoter, along with 4 sgRNA (single guide RNA) targeting human CD47 (NM_198793.2) driven by a U6 promoter._x000D_
Note: unlike human CD47 CRISPR/Cas9 Lentivirus (Integrating) (BPS Bioscience, #78056), the human CD47 CRISPR/Cas9 Lentivirus (Non-Integrating) is made with a mutated Integrase, resulting in only transient expression of the Cas9 and CD47 targeting sgRNA. While this may minimize potential off-targeting risks due to either prolonged expression or integration of the Cas9, puromycin selection should not be used for more than 48 hours post-transduction, which may lower knockout efficiency.

CRBN CRISPR/Cas9 Lentivirus (Non-Integrating)

78518 500 µl x 2
EUR 995
Description: Cereblon (CRBN) forms an E3 ubiquitin ligase complex which is responsible for ubiquitinating proteins that regulate various developmental processes. CRBN also binds to Calcium Activated Potassium Channel subunit alpha-1 (KCNMA1) to regulate ion transport. Moreover, mutations in CRBN may play an underlying role in tumor cells acquiring resistance to immunotherapy.The CRBN CRISPR/Cas9 Lentiviruses are replication incompetent, HIV-based VSV-G pseudo-typed lentiviral particles that are ready to transduce into almost all types of mammalian cells, including primary and non-dividing cells. The particles contain a CRISPR/Cas9 gene driven by an EF1a promoter, along with 5 sgRNA (single guide RNA) targeting human CRBN.The non-integrating lentivirus is made with a mutated integrase, resulting in only transient expression of the Cas9 and sgRNA. Although using the non-integrating lentivirus results in lower knockdown efficiency, the Cas9 is not permanently expressed, which lowers the risk of off-targeting, and there are no random integrations into the cell's genome. Knockout cell lines can still be generated following cell sorting or limited dilution, because even though the Cas9 and sgRNA expression is transient, the changes in the genomic DNA from the Cas9 nuclease activity and NHEJ repair are permanent.

CTLA4 CRISPR/Cas9 Lentivirus (Non-Integrating)

78061 500 µl x 2
EUR 995
Description: CTLA4 (Cytotoxic T-Lymphocyte Associated Protein), also known as CD152, is a protein receptor that functions as an immune checkpoint. It is expressed by activated T-cells and transmits an inhibitory signal to T-cells. CTLA4 is homologous to the T-cell co-stimulatory protein CD28, and both molecules bind to CD80 (B7-1) and CD86 (B7-2) on antigen-presenting cells. CTLA4 binds CD80 and CD86 with greater affinity and avidity than CD28, thus enabling it to out-compete CD28 for its ligands and act as an "off" switch when bound to CD80 or CD86. CTLA4 is an important immunotherapy target for the treatment of cancer and autoimmune diseases._x000D_
The CTLA4 CRISPR Lentiviruses are replication incompetent, HIV-based VSV-G pseudo-typed lentiviral particles that are ready to be transduced into almost all types of mammalian cells, including primary and non-dividing cells. The particles contain a CRISPR/Cas9 gene driven by an EF1a promoter, along with 4 sgRNA (single guide RNA) targeting human CTLA4, GenBank Accession #NM_005214, driven by a U6 promoter._x000D_
Note: Unlike human CTLA4 CRISPR/Cas9 Lentivirus (Integrating) (BPS Bioscience, #78054), the Human CTLA4 CRISPR/Cas9 Lentivirus (Non-Integrating) is made with a mutated Integrase, resulting in only transient expression of the Cas9 and CTLA4 targeting sgRNA. While this may minimize potential off-targeting risks due to either prolonged expression or integration of the Cas9, puromycin selection should not be used for more than 48 hours post-transduction, which may lower knockout efficiency.

TIGIT CRISPR/Cas9 Lentivirus (Non-Integrating)

78065 500 µl x 2
EUR 995
Description: TIGIT (T-cell immunoreceptor with Ig and ITIM domains; VSTM3; VSIG9) is a co-inhibitory receptor that is highly expressed in Natural Killer (NK) cells and activated CD4+, CD8+, and regulatory T-cells. Interaction with the Poliovirus Receptor (PVR; CD155) on antigen presenting cells, such as dendritic cells, recruits either the Src homology (SH) domain-containing tyrosine phosphatases SHP1 and SHP2, or the Inositol phosphatase SHIP1 and SHIP2, to the TIGIT ITIM domain. This increases IL-10 release and suppresses NF-κB and NFAT T-cell receptor (TCR) signaling, which blocks T-cell proliferation and cytokine production. TIGIT also serves as a competitive inhibitor of CD226, a costimulatory receptor for CD155. TIGIT-targeting antibodies which block this T-cell intrinsic inhibitory effect have shown enhanced anti-tumor and anti-viral functions in preclinical studies._x000D_
The TIGIT CRISPR Lentiviruses are replication incompetent, HIV-based VSV-G pseudo-typed lentiviral particles that are ready to be transduced into almost all types of mammalian cells, including primary and non-dividing cells. The particles contain a CRISPR/Cas9 gene driven by an EF1a promoter, along with 4 sgRNA (single guide RNA) targeting human TIGIT (GenBank Accession #NM_173799) driven by a U6 promoter (Figures 1 and 2)._x000D_Note: unlike human TIGIT CRISPR/Cas9 Lentivirus (Integrating) (BPS Bioscience, #78058), the human TIGIT CRISPR/Cas9 Lentivirus (Non-Integrating) is made with a mutated Integrase, resulting in only transient expression of the Cas9 and TIGIT targeting sgRNA. While this may minimize potential off-targeting risks due to either prolonged expression or integration of the Cas9, puromycin selection should not be used for more than 48 hours post-transduction, which may lower knockout efficiency.

CIITA (Human) CRISPR/Cas9 Lentivirus (Integrating)

78435 500 µl x 2
EUR 795
Description: CIITA (class II major histocompatibility complex transactivator) acts as a coactivator for MHC (major histocompatibility complex) class II-specific gene expression and negatively regulates the IL-4 gene promoter during T cell differentiation. IFN-γ (interferon-gamma) induces CIITA gene expression via JAK1 (Janus kinase 1) and Stat1 (Signal transducer and activator of transcription 1) pathways. The GTP-binding and acidic, proline-serine threonine-rich regions appear to be required for CIITA activity. Defects of CIITA has been implicated as causes of bare lymphocyte syndrome (BLS), which is characterized by the absence of MHC class II transcription and severe immunodeficiencies.The CIITA CRISPR/Cas9 Lentiviruses are replication incompetent, HIV-based, VSV-G pseudotyped lentiviral particles that are ready to infect almost all types of mammalian cells, including primary and non-dividing cells. The particles contain a CRISPR/Cas9 gene driven by an EF1a promoter, along with 5 sgRNA (single guide RNAs) targeting human CIITA driven by a U6 promoter.The integrating lentivirus integrates randomly into the cellular genome to express both Cas9 and the sgRNA. Puromycin selection forces high expression levels of both Cas9 and the sgRNA, and can be used with the integrating lentivirus to quickly and easily achieve high knockdown efficiencies in a cell pool. Efficiencies will depend on the cell type and the gene of interest.

NLRP3 CRISPR/Cas9 Lentivirus (Non-Integrating)

78546 500 µl x 2
EUR 795
Description: NLR family Pyrin domain containing 3 (NLRP3) is expressed in macrophages and is a component of inflammasomes. NLRP3 detects uric acid and extracellular ATP in damaged tissue and interacts with a pro-apoptotic protein that recruits caspases. This complex is also an upstream activator of NF-κB signaling and triggers an immune response as part of the innate immune system. Mutations in NLRP3 are known to cause autoinflammatory and neuroinflammatory diseases such as Alzheimer's, Parkinson's, and prion disease. The NLRP3 CRISPR/Cas9 Lentiviruses are replication incompetent, HIV-based VSV-G pseudo-typed lentiviral particles ready to be transduced into most  types of mammalian cells, including primary and non-dividing cells. The particles contain a CRISPR/Cas9 gene driven by an EF1a promoter, along with 5 sgRNA (single guide RNA) targeting human NLRP3 (Figure 1 and Table 1), allowing the knockdown of NLRP3 in transduced cellsThe non-integrating lentivirus is made with a mutated integrase, resulting in only transient expression of the Cas9 and sgRNA. Although using the non-integrating lentivirus results in lower knockdown efficiency, the Cas9 protein is not permanently expressed, which lowers the risk of off-targeting, and there are no random integrations into the cell's genome Despite transient expression of Cas9 and sgRNA, knockout cell lines can be generated using cell sorting or limiting dilution due to the permanent changes in the genomic DNA from the Cas9 nuclease activity and NHEJ repair. 

Kinase (Human) CRISPR/Cas9 Lentivirus (Integrating)

78488 200 µl x 2
EUR 395
Description: To order a CRISPR/Cas9 lentivirus to knockout a kinase of interest, select the Gene Symbol of the kinase in the ordering window (for example, select AKT1 if ordering the lentivirus to knockout kinase AKT1). Download the table to view all available kinases.The Kinase CRISPR/Cas9 lentivirus is designed to target a specific kinase of interest for knockout. The replication-incompetent, HIV-based, VSV-G pseudotyped lentiviral particles are ready to infect almost all types of mammalian cells, including primary and non-dividing cells. The SIN lentiviral backbone contains the Cas9 gene (Streptococcus pyogenes CRISPR associated protein 9) driven by an EF1a promoter, an sgRNA driven by a U6 promoter, and a puromycin selection marker. Each vial of lentivirus consists of a mixture of lentiviral particles targeting 5 different sgRNAs per gene.The lentivirus integrates randomly into the cellular genome to express both Cas9 and the sgRNAs. Because it contains Cas9, the lentivirus can be used in any target cell regardless of whether the cells already express Cas9. Puromycin selection ensures high expression of both Cas9 and the sgRNAs. Knockout efficiencies will depend on the cell type and the gene of interest. Stable CRISPR-Cas9 knockout cell lines can also be generated following limiting dilution.

TGFBR2 CRISPR/Cas9 Lentivirus (Non-Integrating)

78536 500 µl x 2
EUR 995
Description: Transforming growth factor beta receptor 2 (TGFBR2) encodes the TGF-β receptor protein, a transmembrane protein that forms a heterodimeric complex with other receptor proteins and binds TGF-β. This receptor/ligand complex phosphorylates proteins which regulate cell proliferation, cell cycle arrest, wound healing, and immunosuppression. Mutations in TGFBR2 have been linked with Marfan syndrome and the development of various types of tumors.The TGFBR2 CRISPR/Cas9 Lentiviruses are replication incompetent, HIV-based VSV-G pseudotyped lentiviral particles ready to infect most types of mammalian cells, including primary and non-dividing cells. The particles contain a CRISPR/Cas9 gene driven by an EF1a promoter, along with 5 sgRNA (single guide RNA) targeting human TGFBR2 (Figure 1 and Table 1).The TGFRBR2 CRISPR/Cas9 non-integrating lentivirus is made with a mutated integrase, resulting in only transient expression of Cas9 and sgRNA. Although using the non-integrating lentivirus results in lower knockdown efficiency, the Cas9 protein is not permanently expressed, which lowers the risk of off-targeting, and there are no random integrations into the cell's genome. Despite transient expression of Cas9 and sgRNA, knockout cell lines can still be generated using cell sorting or limiting dilution due to the permanent changes in the genomic DNA from the Cas9 nuclease activity and NHEJ repair.

FCGR2A CRISPR/Cas9 Lentivirus (Non-Integrating)

78538 500 µl x 2
EUR 995
Description: Fc Gamma Receptor 2A (also known as CD32A, Fc-gamma RIIa, FcgRIIa) is a low affinity Fc receptor for immunoglobulin G, encoded by the FCGR2A gene. Fc Gamma Receptor 2A is a cell surface receptor that is expressed on a variety of immune cells such as macrophages and neutrophils. It is involved in phagocytosis and in the clearing of spent immune complexes from the circulation. A polymorphism in FCGR2A has been associated with increased risks of nephritis and lupus.The FCGR2A CRISPR/Cas9 Lentiviruses are replication incompetent, HIV-based VSV-G pseudotyped lentiviral particles that are ready to infect most types of mammalian cells, including primary and non-dividing cells. The particles contain a CRISPR/Cas9 gene driven by an EF1a promoter, along with 5 sgRNA (single guide RNA) targeting human FCGR2A.The non-integrating lentivirus is made with a mutated integrase, resulting in only transient expression of Cas9 and sgRNA. Although using the non-integrating lentivirus results in lower knockdown efficiency, Cas9 is not permanently expressed, which lowers the risk of off-targeting, and there are no random integrations into the cell's genome. Despite transient expression of Cas9 and sgRNA, knockout cell lines can still be generated using cell sorting or limiting dilution due to the permanent changes in the genomic DNA from the Cas9 nuclease activity and NHEJ repair.

Cas9 (CMV, Bsd) Integrase-Deficient Lentivirus

IDLV009 1x10^7 IFU/ml x 200ul
EUR 276.5
Description: Integrase-Deficient Lentivirus expressing human codon CAS9 endonuclease under CMV promoter, containing Blasticidin antibiotic marker, provided in DMEM medium with 10% FBS and 60ug/ml of polybrene.

Cas9 (CMV, Neo) Integrase-Deficient Lentivirus

IDLV011 1x10^7 IFU/ml x 200ul
EUR 276.5
Description: Integrase-Deficient Lentivirus expressing human codon CAS9 endonuclease under CMV promoter, containing Neomycin antibiotic marker, provided in DMEM medium with 10% FBS and 60ug/ml of polybrene.

Cas9 (CMV, Zeo) Integrase-Deficient Lentivirus

IDLV021 1x10^7 IFU/ml x 200ul
EUR 276.5
Description: Integrase-Deficient Lentivirus expressing human codon CAS9 endonuclease under CMV promoter, containing Zeocin antibiotic marker, provided in DMEM medium with 10% FBS and 60ug/ml of polybrene.

Cas9 (CMV, Puro) Integrase-Deficient Lentivirus

IDLV007 1x10^7 IFU/ml x 200ul
EUR 276.5
Description: Integrase-Deficient Lentivirus expressing human codon CAS9 endonuclease under CMV promoter, containing Puromycin antibiotic marker, provided in DMEM medium with 10% FBS and 60ug/ml of polybrene.

Cas9 (EF1a, Bsd) Integrase-Deficient Lentivirus

IDLV010 1x10^7 IFU/ml x 200ul
EUR 276.5
Description: Integrase-Deficient Lentivirus expressing human codon CAS9 endonuclease under EF1a promoter, containing Blasticidin antibiotic marker, provided in DMEM medium with 10% FBS and 60ug/ml of polybrene.

Cas9 (EF1a, Neo) Integrase-Deficient Lentivirus

IDLV012 1x10^7 IFU/ml x 200ul
EUR 276.5
Description: Integrase-Deficient Lentivirus expressing human codon CAS9 endonuclease under EF1a promoter, containing Neomycin antibiotic marker, provided in DMEM medium with 10% FBS and 60ug/ml of polybrene.

Cas9 (EF1a, Zeo) Integrase-Deficient Lentivirus

IDLV022 1x10^7 IFU/ml x 200ul
EUR 276.5
Description: Integrase-Deficient Lentivirus expressing human codon CAS9 endonuclease under EF1a promoter, containing Zeocin antibiotic marker, provided in DMEM medium with 10% FBS and 60ug/ml of polybrene.

Cas9 (EF1a, Puro) Integrase-Deficient Lentivirus

IDLV008 1x10^7 IFU/ml x 200ul
EUR 276.5
Description: Integrase-Deficient Lentivirus expressing human codon CAS9 endonuclease under EF1a promoter, containing Puromycin antibiotic marker, provided in DMEM medium with 10% FBS and 60ug/ml of polybrene.

PD-1 CRISPR/Cas9 Lentivirus (Non-Integrating)

78059 500 µl x 2
EUR 995
Description: The binding of Programmed Cell Death Protein 1 (PD-1), a receptor expressed on activated T-cells, to its ligands, PD-L1 and PD-L2, negatively regulates immune responses. PD-1 ligands are found on most cancers, and the PD-1:PD-L1/2 interaction inhibits T-cell activity and enables cancer cells to escape immune surveillance. The PD-1:PD-L1/2 pathway is also involved in regulating autoimmune responses, making these proteins promising therapeutic targets for a number of cancers, as well as multiple sclerosis, arthritis, lupus, and type I diabetes. The PD-1 CRISPR Lentiviruses are replication incompetent, HIV-based VSV-G pseudo-typed lentiviral particles that are ready to be transduced into almost all types of mammalian cells, including primary and non-dividing cells. The particles contain a CRISPR/Cas9 gene driven by an EF1a promoter, along with 4 sgRNA (single guide RNA) targeting human PD-1 (Programmed Cell Death 1, PDCD1, CD279, GenBank Accession #NM_005018) driven by a U6 promoter. The non-integrating lentivirus is made with a mutated integrase, resulting in only transient expression of the Cas9 and sgRNA. Although using the non-integrating lentivirus results in lower knockdown efficiency, the Cas9 isn't permanently expressed, which lowers the risk of off-targeting, and there are no random integrations into the cell's genome. Knockout cell lines can still be generated following cell sorting or limited dilution, because even though the Cas9 and sgRNA expression is transient, the changes in the genomic DNA from the Cas9 nuclease activity and NHEJ repair are permanent. 

CBL-B (Human) CRISPR/Cas9 Lentivirus (Integrating)

78343 500 µl x 2
EUR 795
Description: CBL-B is an E3 ubiquitin-protein ligase which has been identified as a negative regulator of T-cell activation. Using CRISPR/Cas9 to inactivate CBL-B has been shown to be sufficient to inhibit T-cell expansion.The CBL-B CRISPR/Cas9 Lentiviruses are replication incompetent, HIV-based, VSV-G pseudotyped lentiviral particles that are ready to infect almost all types of mammalian cells, including primary and non-dividing cells. The particles contain a CRISPR/Cas9 gene driven by an EF1a promoter, along with 5 sgRNA (single guide RNAs) targeting human CBL-B driven by a U6 promoter.The integrating lentivirus integrates randomly into the cellular genome to express both Cas9 and the sgRNA. Puromycin selection forces high expression levels of both Cas9 and the sgRNA, and can be used with the integrating lentivirus to quickly and easily achieve high knockdown efficiencies in a cell pool. Efficiencies may vary, depending on the cell type and the gene of interest.

CD5 (Human) CRISPR/Cas9 Lentivirus (Non-Integrating)

78198 500 µl x 2
EUR 995
Description: The CD5 CRISPR Lentiviruses are replication incompetent, HIV-based VSV-G  pseudotyped lentiviral particles that are ready to  infect almost all types of mammalian cells, including primary and non-dividing cells. The particles contain a CRISPR/Cas9 gene driven by an EF1a promoter, along with 5 sgRNA (single guide RNA) targeting human CD5 driven by a U6 promoter.The integrating lentivirus integrates randomly into the  cellular genome to express both Cas9 and the sgRNA. Puromycin selection forces high expression levels of both Cas9 and the sgRNA, and can be used with the integrating lentivirus to quickly and easily achieve high knockdown efficiencies in a cell pool. Efficiencies may vary, depending on the cell type and the gene of interest.

B2M (Human) CRISPR/Cas9 Lentivirus (Non-Integrating)

78341 500 µl x 2
EUR 995
Description: Beta-2 Microglobulin (B2M) is a required component of Major Histocompatibility Complex (MHC) class 1 molecules, which present peptide fragments from within the cell to cytotoxic T-cells as part of the adaptive immune system. The B2M CRISPR/Cas9 Lentiviruses are replication incompetent, HIV-based, VSV-G pseudotyped lentiviral particles that are ready to infect almost all types of mammalian cells, including primary and non-dividing cells. The particles contain a CRISPR/Cas9 gene driven by an EF1a promoter, along with 5 sgRNA (single guide RNAs) targeting human B2M driven by a U6 promoter.The integrating lentivirus integrates randomly into the cellular genome to express both Cas9 and the sgRNA. Puromycin selection forces high expression levels of both Cas9 and the sgRNA, and can be used with the integrating lentivirus to quickly and easily achieve high knockdown efficiencies in a cell pool. Efficiencies will depend on the cell type and the gene of interest.

Cas9 (CMV, Zeo) lentiviral particles, Concentrated Lentivirus

LVP1391-PBS 1x10^8 IFU/ml x 200ul
EUR 455
Description: concentrated CAS9 endonuclease expression lentivirus under CMV promoter, containing Zeocin antibiotic marker.

Cas9 (EF1a, Zeo) lentiviral particles, Concentrated Lentivirus

LVP1392-PBS 1x10^8 IFU/ml x 200ul
EUR 455
Description: concentrated CAS9 endonuclease expression lentivirus under EF1a promoter, containing Zeocin antibiotic marker.

CIITA (Human) CRISPR/Cas9 Lentivirus (Non-integrating)

78434 500 µl x 2
EUR 995
Description: CIITA (class II major histocompatibility complex transactivator) acts as a coactivator for MHC (major histocompatibility complex) class II-specific gene expression and negatively regulates the IL-4 gene promoter during T cell differentiation. IFN-γ (interferon-gamma) induces CIITA gene expression via Janus kinase 1) and Stat1 (Signal transducer and activator of transcription 1) pathways. The GTP-binding and acidic, proline-serine threonine-rich regions appear to be required for CIITA activity. Defects of CIITA has been implicated as causes of bare lymphocyte syndrome (BLS), which is characterized by the absence of MHC class II transcription and severe immunodeficiencies.The CIITA CRISPR/Cas9 Lentiviruses are replication incompetent, HIV-based, VSV-G pseudotyped lentiviral particles that are ready to infect almost all types of mammalian cells, including primary and non-dividing cells. The particles contain a CRISPR/Cas9 gene driven by an EF1a promoter, along with 5 sgRNA (single guide RNAs) targeting human CIITA driven by a U6 promoter.Unlike CIITA CRISPR/Cas9 Lentivirus (Integrating) (BPS Bioscience #78435), the CIITA CRISPR/Cas9 Lentivirus (Non-Integrating) is made with a mutated Integrase, resulting in only transient expression of the Cas9 and CIITA targeting sgRNA. This transient expression minimizes potential off-target effects caused by either prolonged expression or random integration of Cas9 and the sgRNA. A short round of puromycin selection right after transduction may increase knockout efficiency, however puromycin should not be used for more than 48 hours post-transduction due to the transient nature of expression using the non-integrating lentivirus.

Cas9 (CMV, GFP-Bsd) Integrase-Deficient Lentivirus

IDLV017 1x10^7 IFU/ml x 200ul
EUR 276.5
Description: Integrase-Deficient Lentivirus expressing human codon CAS9 endonuclease under CMV promoter, containing GFP-Blasticidin fusion dual marker, provided in DMEM medium with 10% FBS and 60ug/ml of polybrene.

Cas9 (CMV, RFP-Bsd) Integrase-Deficient Lentivirus

IDLV019 1x10^7 IFU/ml x 200ul
EUR 276.5
Description: Integrase-Deficient Lentivirus expressing human codon CAS9 endonuclease under CMV promoter, containing RFP-Blasticidin fusion dual marker, provided in DMEM medium with 10% FBS and 60ug/ml of polybrene.

Cas9 (CMV, GFP-Puro) Integrase-Deficient Lentivirus

IDLV013 1x10^7 IFU/ml x 200ul
EUR 276.5
Description: Integrase-Deficient Lentivirus expressing human codon CAS9 endonuclease under CMV promoter, containing GFP-Puromycin fusion dual marker, provided in DMEM medium with 10% FBS and 60ug/ml of polybrene.

Cas9 (CMV, RFP-Puro) Integrase-Deficient Lentivirus

IDLV015 1x10^7 IFU/ml x 200ul
EUR 276.5
Description: Integrase-Deficient Lentivirus expressing human codon CAS9 endonuclease under CMV promoter, containing RFP-Puromycin fusion dual marker, provided in DMEM medium with 10% FBS and 60ug/ml of polybrene.

Cas9 (EF1a, GFP-Bsd) Integrase-Deficient Lentivirus

IDLV018 1x10^7 IFU/ml x 200ul
EUR 276.5
Description: Integrase-Deficient Lentivirus expressing human codon CAS9 endonuclease under EF1a promoter, containing GFP-Blasticidin fusion dual marker, provided in DMEM medium with 10% FBS and 60ug/ml of polybrene.

Cas9 (EF1a, RFP-Bsd) Integrase-Deficient Lentivirus

IDLV020 1x10^7 IFU/ml x 200ul
EUR 276.5
Description: Integrase-Deficient Lentivirus expressing human codon CAS9 endonuclease under EF1a promoter, containing RFP-Blasticidin fusion dual marker, provided in DMEM medium with 10% FBS and 60ug/ml of polybrene.

Cas9 (EF1a, GFP-Puro) Integrase-Deficient Lentivirus

IDLV014 1x10^7 IFU/ml x 200ul
EUR 276.5
Description: Integrase-Deficient Lentivirus expressing human codon CAS9 endonuclease under EF1a promoter, containing GFP-Puromycin fusion dual marker, provided in DMEM medium with 10% FBS and 60ug/ml of polybrene.
Furthermore, we are going to briefly summarise a number of the limitations of present liver-directed gene remedy approaches and potential methods of overcoming them.

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