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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
MON1/CALCIUM CAFFEINE ZINC SENSITIVITY1 (CCZ1)-mediated Rab7 activation was indispensable for vacuolar trafficking of tapetum degradation-related cysteine proteases.
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.
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.
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).
clear effect of subcutaneous zoledronic acid administration in vivo on the prenylation of Rab1A (show RAB1A Proteins), Rab5B (show RAB5B Proteins), Rab7A and Rab14 (show RAB14 Proteins) in mouse peritoneal macrophages, confirming that systemic treatment with bisphosphonate drug can inhibit prenylation in myeloid cells in vivo outside the skeleton.
increased endolysosomal iron causes cell death associated with increased cytosolic oxidative stress as well as autophagic impairments, and these effects are subject to modulation by endolysosomal ion channel activity in a RAB7A-dependent manner
WDR91 serves as a Rab7 (show RAB7B Proteins) effector that is essential for neuronal development by facilitating endosome conversion in the endosome-lysosome pathway.
The Vici syndrome protein EPG5 is a Rab7 (show RAB7B Proteins) effector that determines the fusion specificity of autophagosomes with late endosomes/lysosomes.
up-regulation of RAB7A reported in Alzheimer's disease, could contribute to the extracellular accumulation of pathological TAU
Rab7 (show RAB7B Proteins) 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.
Rab7a depletion decreases the amount of active Rac1 but not its abundance and reduces the number of cells with vimentin (show VIM Proteins) filaments facing the wound, indicating that Rab7a has a role in the orientation of vimentin (show VIM Proteins) filaments during migration
The study highlighted the importance of a phosphorylation/dephosphorylation switch in controlling timely Rab7 (show RAB7B Proteins) localization and activity on endosomes.
show that the maturation of Mtb (show NCAPG2 Proteins)-containing autophagosomes into autolysosomes required recruitment of the late endosome marker RAB7 (show RAB7B Proteins), forming the intermediate compartment amphisomes
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