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Human RAB7A Protein expressed in HEK-293 Cells - ABIN2730367
Ye, Gao, Tian, Yearsley, Lange, Robertson, Barsky: Early to intermediate steps of tumor embolic formation involve specific proteolytic processing of E-cadherin regulated by Rab7. in Molecular cancer research : MCR 2012
control of RAB7 (show RAB7B Proteins) activity is not required for the recycling of retromer-dependent cargoes, but instead enables the correct sorting of the autophagy related transmembrane protein ATG9a (show ATG9A Proteins) and autophagosome formation around damaged mitochondria during Parkin (show PARK2 Proteins)-mediated mitophagy.
The authors demonstrate that RABGEF1 (show RABGEF1 Proteins), the upstream factor of the endosomal Rab GTPase (show RAB6A Proteins) cascade, is recruited to damaged mitochondria via ubiquitin binding downstream of Parkin (show PARK2 Proteins). RABGEF1 (show RABGEF1 Proteins) directs the downstream Rab (show HRB Proteins) proteins, RAB5 (show RAB5A Proteins) and RAB7A, to damaged mitochondria, whose associations are further regulated by mitochondrial Rab (show HRB Proteins)-GAPs.
these findings reveal a new role of Rab7a in Endoplasmic Reticulum (ER)homeostasis, and indicate that genetic and pharmacological ER stress manipulation may restore ER morphology in Rab7a silenced cells.
Mitochondria-lysosome contacts regulate mitochondrial fission via RAB7 (show RAB7B Proteins) GTP (show AK3 Proteins) hydrolysis
This paper identifies a CD44s-interacting small GTPase (show RACGAP1 Proteins), Rab7A, and shows that CD44s inhibits Rab7A-mediated EGFR (show EGFR Proteins) trafficking to lysosomes and subsequent degradation.
results indicate that Rab7 (show RAB7B Proteins) palmitoylation is required for the spatiotemporal recruitment of retromer and efficient endosome-to-trans-Golgi network trafficking of the lysosomal sorting receptors.
Hepatitis C virus (HCV) modifies cellular trafficking by cleaving Rab interacting lysosomal protein (RILP (show RILP Proteins)), which serves to redirect ras-related protein Rab-7 (Rab7 (show RAB7B Proteins))-containing vesicles to a kinesin-dependent trafficking mode promoting virion secretion.
Rab7 (show RAB7B Proteins) GTPase (show RACGAP1 Proteins) plays a key role in regulating MDSCs development, differentiation, trans-endothelial migration, anti-tumor immunity and direct tumor stimulation through physical interaction with the mTOR (show FRAP1 Proteins) complexes.
The results were indicative that rabies virus N proficiently colocalized with Rab5 (show RAB5A Proteins)/EEA1 (show EEA1 Proteins) and Rab7 (show RAB7B Proteins)/LAMP1 (show LAMP1 Proteins) in both cell lines at 24 and 48 h post-infection, while N titers significantly decreased in early infection of rabies virus.
We provide evidence here that Rab7 (show RAB7B Proteins) is a substrate of Src kinase (show CSK Proteins), and is tyrosine-phosphorylated by Src (show SRC Proteins), withY183 residue of Rab7 (show RAB7B Proteins) being the optimal phosphorylation site for Src (show SRC Proteins). Further investigations demonstrated that the tyrosine phosphorylation of Rab7 (show RAB7B Proteins) depends on the guanine nucleotide binding activity of Rab7 (show RAB7B Proteins) and the activity of Src kinase (show CSK Proteins).
MON1/CALCIUM CAFFEINE ZINC SENSITIVITY1 (CCZ1)-mediated Rab7 activation was indispensable for vacuolar trafficking of tapetum degradation-related cysteine proteases.
High Rab7 expression is associated with tumor growth and metastasis.
WDR91 serves as a Rab7 effector that is essential for neuronal development by facilitating endosome conversion in the endosome-lysosome pathway.
Vps34 (show PIK3C3 Proteins) has a previously unknown role in regulating Rab7 activity and late endosomal trafficking.
Rab7 accumulated in GCase (show GBA Proteins) deficient cells, supporting the notion that lysosomal recycling is impaired. Since recombinant GCase (show GBA Proteins) can reverse ALR (show GFER Proteins) impairment, we anticipate that strategies to restore GCase (show GBA Proteins) activity in the brains of both sporadic patients with PD and those with GBA1 (show GBA Proteins) mutations will improve autophagy lysosomal pathway, preventing the accumulation of a-synuclein and spread of pathology.
The up-regulation of Rab11 (show RAB11A Proteins), Rab7, or RILP (show RILP Proteins), but not its truncated form RILP (show RILP Proteins)-C33 (show CD82 Proteins), rescued LAMP2A-defective trafficking in cystinosis, whereas dominant-negative Rab11 (show RAB11A Proteins) or Rab7 impaired LAMP2A trafficking.
The inhibition of autophagosome-lysosome fusion induced by SapM is dependent on the interaction between SapM and Rab7.
Prion (show PRNP Proteins) infection impairs lysosomal degradation capacity by interfering with rab7 membrane attachment in neuronal cells.
photoreceptor outer segments vesicles engulfed through Lyar-dependent pathway were targeted to phagosomes and colocalized with phagosome marker Rab7
B cell Rab7 mediates induction of activation-induced cytidine deaminase (show AICDA Proteins) expression and class-switching in T-dependent and T-independent antibody responses.
CREG1 (show CREG1 Proteins) deficiency influenced the maturation of lysosomes and reduced the espression of Rab7, which might be involved in CREG1 (show CREG1 Proteins)-induced cardiomyocyte autophagy.
Data provide new insight into how disease-associated alterations in Rab7 protein disrupt cellular function in vertebrate sensory neurons. Moreover, findings suggest that defects in axon development may be a previously unrecognized component of Charcot-Marie-Tooth2b disease.
The established transgenic lines ubiquitously express EGFP fusions of Rab5c (show Rab5c Proteins) (early endosomes), Rab11a (show RAB11A Proteins) (recycling endosomes), and Rab7 (late endosomes) to study localization and dynamics during development.
RAB family members are small, RAS-related GTP-binding proteins that are important regulators of vesicular transport. Each RAB protein targets multiple proteins that act in exocytic / endocytic pathways. This gene encodes a RAB family member that regulates vesicle traffic in the late endosomes and also from late endosomes to lysosomes. This encoded protein is also involved in the cellular vacuolation of the VacA cytotoxin of Helicobacter pylori. Mutations at highly conserved amino acid residues in this gene have caused some forms of Charcot-Marie-Tooth (CMT) type 2 neuropathies.
RAB7, member RAS oncogene family
, Ras-associated protein RAB7
, ras-related protein Rab-7a
, ras-related protein BRL-RAS
, ras-related protein p23
, GTP-binding protein (rab7)
, ras-related protein Rab-7
, RAB7A, member RAS oncogene family
, rab7A protein
, ras-related protein rab-7a