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Validated All-in-One™ qPCR Primer for RAB4A(NM_004578.3) Search again
Product ID:
HQP016049
(click here to view gene annotation page)
Species:
Human
Symbol:
Alias:
HRES-1, HRES-1/RAB4, HRES1, RAB4
Gene Description:
RAB4A, member RAS oncogene family
Target Gene Accession:
NM_004578.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Gene References into function
- Rab coupling protein (RCP), a novel Rab4 and Rab11 effector protein
- Data suggest that abnormal membrane recycling in Niemann-Pick type A and C lipid storage disease fibroblasts results from specific inhibition of rab4 function by excess cholesterol in early endosomes.
- In contrast to Rab11, Rab4 is not involved in exocytosis
- Rab4 specific residue His39 modulates the nucleotide binding pocket giving rise to a reduced rate for nucleotide hydrolysis and exchange
- critical element that regulates epithelial sodium channel (ENaC) function by GTP-GDP recycling and concomitant changes in ENaC expression at the cell surface and in intracellular pool
- The study suggests that Rab4 regulates the channel through multiple mechanisms that include protein-protein interaction, GTP/GDP exchange, and channel protein trafficking.
- CT229 of Chlamydia trachomatis interacts with and recruits Rab4A to the inclusion membrane and therefore may play a role in regulating the intracellular trafficking or fusogenicity of the chlamydial inclusion.
- Regulation of CD4 expression via recycling by HRES-1/RAB4 controls susceptibility to HIV infection
- elevated [5HT](ex)"paralyzes" the translocation of SERT from intracellular locations to the plasma membrane by controlling transamidation and Rab4-GTP formation
- Both phosphorylated and nonphosphorylated MOR internalize via Rab5-dependent pathway after agonist stimulation, and the phosphorylated and nonphosphorylated MORs recycle through distinct vesicular trafficking pathways mediated by Rab4 and Rab11.
- Cyclic AMP-mediated phosphoinositide-3-kinase-independent activation of Rab4 facilitates Ntcp translocation in a hepatoma cell line.
- activation of mTOR causes the loss of TCRzeta in lupus T cells through HRES-1/Rab4-dependent lysosomal degradation.
