Arhgap44 (NM_175003) Mouse Tagged ORF Clone Lentiviral Particle

SKU MR210534L4V

Lenti ORF particles, Arhgap44 (GFP-tagged) - Mouse Rho GTPase activating protein 44 (Arhgap44), transcript variant 2, 200ul, >10^7 TU/mL

Product Data

• Type: Mouse Tagged ORF Clone Lentiviral Particle
• Tag: mGFP
• Target Symbol: Arhgap44
• Synonyms: 6330543G20; AI840762; AU040829; AW493732; Rich2
• Vector: pLenti-C-mGFP-P2A-Puro
• Mammalian Cell Selection: Puromycin
• Sequence Data:
  ORF Nucleotide Sequence

  The ORF insert of this clone is exactly the same as(MR210534).
• ACCN: NM_175003
• ORF Size: 2292 bp
• OTI Disclaimer: The molecular sequence of this clone aligns with the gene accession number as a point of reference only. However, individual transcript sequences of the same gene can differ through naturally occurring variations (e.g. polymorphisms), each with its own valid existence. This clone is substantially in agreement with the reference, but a complete review of all prevailing variants is recommended prior to use. More info
• OTI Annotation: This clone was engineered to express the complete ORF with an expression tag. Expression varies depending on the nature of the gene.
• Shipping: Dry Ice

Reference Data

• RefSeq: NM_175003.2, NP_778168.2
• RefSeq Size: 4099 bp
• RefSeq ORF: 2295 bp
• Locus ID: 216831
• UniProt ID: Q5SSM3
• Cytogenetics: 11 B3
• Summary: GTPase-activating protein (GAP) that stimulates the GTPase activity of Rho-type GTPases. Thereby, controls Rho-type GTPases cycling between their active GTP-bound and inactive GDP-bound states. Acts as a GAP at least for CDC42 and RAC1 (PubMed:24352656, PubMed:26969129). In neurons, is involved in dendritic spine formation and synaptic plasticity in a specific RAC1-GAP activity (PubMed:23739967, PubMed:24352656, PubMed:26969129). Limits the initiation of exploratory dendritic filopodia. Recruited to actin-patches that seed filopodia, binds specifically to plasma membrane sections that are deformed inward by acto-myosin mediated contractile forces. Acts through GAP activity on RAC1 to reduce actin polymerization necessary for filopodia formation (By similarity). In association with SHANK3, promotes GRIA1 exocytosis from recycling endosomes and spine morphological changes associated to long-term potentiation (PubMed:23739967).[UniProtKB/Swiss-Prot Function]