Arhgdia (NM_133796) Mouse Tagged ORF Clone Lentiviral Particle

CAT#: MR202112L3V

Lenti ORF particles, Arhgdia (Myc-DDK-tagged) - Mouse Rho GDP dissociation inhibitor (GDI) alpha (Arhgdia), 200ul, >10^7 TU/mL

Specifications

Product Data

• Type: Mouse Tagged ORF Clone Lentiviral Particle
• Tag: Myc-DDK
• Symbol: Arhgdia
• Synonyms: 5330430M07Rik; Gdi-1; Rho-GDI; RhoDGI; RhoGDI-1
• Mammalian Cell Selection: Puromycin
• Vector: pLenti-C-Myc-DDK-P2A-Puro
• ACCN: NM_133796
• ORF Size: 615 bp
• Sequence Data:
  ORF Nucleotide Sequence

  The ORF insert of this clone is exactly the same as(MR202112).
• 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.

Reference Data

• RefSeq: NM_133796.5
• RefSeq Size: 2732 bp
• RefSeq ORF: 615 bp
• Locus ID: 192662
• UniProt ID: Q99PT1
• Cytogenetics: 11 E2
• Gene Summary: Controls Rho proteins homeostasis. Regulates the GDP/GTP exchange reaction of the Rho proteins by inhibiting the dissociation of GDP from them, and the subsequent binding of GTP to them. Retains Rho proteins such as CDC42, RAC1 and RHOA in an inactive cytosolic pool, regulating their stability and protecting them from degradation. Actively involved in the recycling and distribution of activated Rho GTPases in the cell, mediates extraction from membranes of both inactive and activated molecules due its exceptionally high affinity for prenylated forms. Through the modulation of Rho proteins, may play a role in cell motility regulation. In glioma cells, inhibits cell migration and invasion by mediating the signals of SEMA5A and PLXNB3 that lead to inactivation of RAC1.[UniProtKB/Swiss-Prot Function]