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Validated All-in-One™ qPCR Primer for RAB5A(NM_004162.4) Search again
Product ID:
HQP016050
(click here to view gene annotation page)
Species:
Human
Symbol:
Alias:
RAB5
Gene Description:
RAB5A, member RAS oncogene family
Target Gene Accession:
NM_004162.4(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
- Expression of a GTPase-hydrolysis-defective rab5a affects lysosome biogenesis by alteration of traffic between lysosomes and endosomes.
- Rab5a regulates fusion between pathogen-containing phagosomes and cytoplasmic organelles in human neutrophils
- an endocytotic catalyst, a tandem regulator of thyroid hormone production
- effect of SARA on rab5-mediated endocytosis
- Rab5a has a P-loop backbone amide group, which is required for catalysis
- dynamin2 and Rab5 have roles in endocytosis of lysophosphatidic acid-coupled LPA1/EDG-2 receptors
- In Rab5 overexpressing cells, the levels of beta-cleaved amyloid precursor protein (APP) carboxyl-terminal fragments (betaCTF), the rate-limiting proteolytic intermediate in Abeta generation, were increased
- increase in the concentration of copper in the medium (189 microM) rapidly induces a redistribution of the MNK protein from early sorting endosomes, positive for Rab5-myc protein, to late endosomes, containing the Rab7-myc protein
- Cell cycle was lengthened by blocking or reducing expression of RAB5A G81R mutation.
- identification of a pathway directly linking the small GTPase Rab5, a key regulator of endocytosis, to signal transduction and mitogenesis via APPL1 and APPL2, two Rab5 effectors
- Guanine nucleotide binding state of rab5 has no bearing on the rate of EGFR endocytosis. However, expression of dominant negative rab5 affects downstream endocytic trafficking by slowing the ligand-induced disappearance of total cellular EGFR.
- Rab5 regulates and coordinates different endocytic mechanisms through its effector Rabankyrin-5
- These results suggest that amyotrophic lateral sclerosis 2 C-terminal like (ALS2CL), a novel ALS2 homologue, modulates Rab5-mediated endosome dynamics in HeLa cells.
- Taken together, these results demonstrate that Rab5 is required for insulin receptor membrane trafficking and signaling.
- We show that EGF relocates to the cell centre in a dynein-dependent fashion, concomitant with the sorting away of transferrin receptor, although it remains in Rab5-positive early endosomes.
- Rab5 participates in the hepatitis C virus RNA replication machinery.
- Rab 5 is required for the cellular entry of dengue and West Nile viruses.
- TSH controls Rab5a activity by promoting its GTP-bound state
- Results suggest that Rab5 and RalA regulate P-gp trafficking between the plasma membrane and an intracellular compartment.
- The crystal structures of human APPL1 N-terminal BAR-PH domain motif, is reported.
- Rab5 activation via amyloid precursor protein signal pathway mediates neuronal apoptosis.
- B coxsackievirus entry depends on occludin and require the activity of Rab34, Ras, and Rab5, GTPases known to regulate macropinocytosis.
- SopB mediates PI(3)P production on the SCV indirectly through recruitment of Rab5 and its effector Vps34.
- Rab5 is a critical regulator of syndecan-1 shedding that serves as an on-off molecular switch through its alternation between the GDP-bound and GTP-bound forms.
- caspase 8 has a role as a modulator of p85alpha Rab5-GAP activity and endosomal trafficking
- Specific residues of RIN1 are required for its interaction with Rab5, binding to the endosomal membranes and subsequent regulation of the fusion reaction.
- Mutations in the Vps9 domain of Rin1 lead to a loss-of-function phenotype, indicating a specific structure-function relationship between Rab5 and Rin1.
