Human VEGFA activation kit by CRISPRa
CAT#: GA105115
VEGFA CRISPRa kit - CRISPR gene activation of human vascular endothelial growth factor A
Find the corresponding CRISPRi Inhibitor Kit
USD 1,290.00
2 Weeks*
USD 379.00
Specifications
Product Data | |
Format | 3gRNAs, 1 scramble ctrl and 1 enhancer vector |
Symbol | VEGFA |
Locus ID | 7422 |
Kit Components | GA105115G1, VEGFA gRNA vector 1 in pCas-Guide-GFP-CRISPRa GA105115G2, VEGFA gRNA vector 2 in pCas-Guide-GFP-CRISPRa GA105115G3, VEGFA gRNA vector 3 in pCas-Guide-GFP-CRISPRa 1 CRISPRa-Enhancer vector, SKU GE100056 1 CRISPRa scramble vector, SKU GE100077 |
Disclaimer | The kit is designed based on the best knowledge of CRISPa SAM technology. The efficiency of the activation can be affected by many factors, including nucleosome occupancy status, chromatin structure and the gene expression level of the target, etc. |
Reference Data | |
RefSeq | NM_001025366, NM_001025367, NM_001025368, NM_001025369, NM_001025370, NM_001033756, NM_001171622, NM_001171623, NM_001171624, NM_001171625, NM_001171626, NM_001171627, NM_001171628, NM_001171629, NM_001171630, NM_001204384, NM_001204385, NM_001287044, NM_003376, NM_001317010 |
Synonyms | MVCD1; VEGF; VPF |
Summary | 'This gene is a member of the PDGF/VEGF growth factor family. It encodes a heparin-binding protein, which exists as a disulfide-linked homodimer. This growth factor induces proliferation and migration of vascular endothelial cells, and is essential for both physiological and pathological angiogenesis. Disruption of this gene in mice resulted in abnormal embryonic blood vessel formation. This gene is upregulated in many known tumors and its expression is correlated with tumor stage and progression. Elevated levels of this protein are found in patients with POEMS syndrome, also known as Crow-Fukase syndrome. Allelic variants of this gene have been associated with microvascular complications of diabetes 1 (MVCD1) and atherosclerosis. Alternatively spliced transcript variants encoding different isoforms have been described. There is also evidence for alternative translation initiation from upstream non-AUG (CUG) codons resulting in additional isoforms. A recent study showed that a C-terminally extended isoform is produced by use of an alternative in-frame translation termination codon via a stop codon readthrough mechanism, and that this isoform is antiangiogenic. Expression of some isoforms derived from the AUG start codon is regulated by a small upstream open reading frame, which is located within an internal ribosome entry site. The levels of VEGF are increased during infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), thus promoting inflammation by facilitating recruitment of inflammatory cells, and by increasing the level of angiopoietin II (Ang II), one of two products of the SARS-CoV-2 binding target, angiotensin-converting enzyme 2 (ACE2). In turn, Ang II facilitates the elevation of VEGF, thus forming a vicious cycle in the release of inflammatory cytokines. [provided by RefSeq, Jun 2020]' |
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KN217312 | VEGFA - human gene knockout kit via CRISPR, HDR mediated |
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KN217312BN | VEGFA - human gene knockout kit via CRISPR, HDR mediated |
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KN217312LP | VEGFA - human gene knockout kit via CRISPR, HDR mediated |
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KN217312RB | VEGFA - human gene knockout kit via CRISPR, HDR mediated |
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KN417312 | VEGFA - KN2.0, Human gene knockout kit via CRISPR, non-homology mediated. |
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