PEX5 Human Gene Knockout Kit (CRISPR)

CAT#: KN402062

PEX5 - KN2.0, Human gene knockout kit via CRISPR, non-homology mediated.

Product Images

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Specifications

Product Data

• Format: 2 gRNA vectors, 1 linear donor
• Donor DNA: EF1a-GFP-P2A-Puro
• Symbol: PEX5
• Locus ID: 5830
• Disclaimer: The kit is designed based on the best knowledge of CRISPR technology. The system has been functionally validated for knocking-in the cassette downstream the native promoter. The efficiency of the knock-out varies due to the nature of the biology and the complexity of the experimental process.

Reference Data

• RefSeq: NM_000319, NM_001131023, NM_001131024, NM_001131025, NM_001131026, NM_001300789, NM_001351124, NM_001351126, NM_001351127, NM_001351128, NM_001351130, NM_001351131, NM_001351132, NM_001351133, NM_001351134, NM_001351135, NM_001351136, NM_001351137, NM_001351138, NM_001351139, NM_001351140
• Synonyms: PBD2A; PBD2B; PTS1-BP; PTS1R; PXR1; RCDP5
• Summary: 'The product of this gene binds to the C-terminal PTS1-type tripeptide peroxisomal targeting signal (SKL-type) and plays an essential role in peroxisomal protein import. Peroxins (PEXs) are proteins that are essential for the assembly of functional peroxisomes. The peroxisome biogenesis disorders (PBDs) are a group of genetically heterogeneous autosomal recessive, lethal diseases characterized by multiple defects in peroxisome function. The peroxisomal biogenesis disorders are a heterogeneous group with at least 14 complementation groups and with more than 1 phenotype being observed in cases falling into particular complementation groups. Although the clinical features of PBD patients vary, cells from all PBD patients exhibit a defect in the import of one or more classes of peroxisomal matrix proteins into the organelle. Defects in this gene are a cause of neonatal adrenoleukodystrophy (NALD), a cause of Zellweger syndrome (ZWS) as well as may be a cause of infantile Refsum disease (IRD). Alternatively spliced transcript variants encoding different isoforms have been identified. [provided by RefSeq, Oct 2008]'