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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 Antibodies) (early endosomes), Rab11a (show RAB11A Antibodies) (recycling endosomes), and Rab7 (late endosomes) to study localization and dynamics during development.
WDR91 serves as a Rab7 effector that is essential for neuronal development by facilitating endosome conversion in the endosome-lysosome pathway.
Vps34 (show PIK3C3 Antibodies) has a previously unknown role in regulating Rab7 activity and late endosomal trafficking.
Rab7 accumulated in GCase (show GBA Antibodies) deficient cells, supporting the notion that lysosomal recycling is impaired. Since recombinant GCase (show GBA Antibodies) can reverse ALR (show GFER Antibodies) impairment, we anticipate that strategies to restore GCase (show GBA Antibodies) activity in the brains of both sporadic patients with PD and those with GBA1 (show GBA Antibodies) mutations will improve autophagy lysosomal pathway, preventing the accumulation of a-synuclein and spread of pathology.
The up-regulation of Rab11 (show RAB11A Antibodies), Rab7, or RILP (show RILP Antibodies), but not its truncated form RILP (show RILP Antibodies)-C33 (show CD82 Antibodies), rescued LAMP2A-defective trafficking in cystinosis, whereas dominant-negative Rab11 (show RAB11A Antibodies) 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 Antibodies) 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 Antibodies) expression and class-switching in T-dependent and T-independent antibody responses.
CREG1 (show CREG1 Antibodies) deficiency influenced the maturation of lysosomes and reduced the espression of Rab7, which might be involved in CREG1 (show CREG1 Antibodies)-induced cardiomyocyte autophagy.
Tropheryma whipplei blocks the switch from Rab5 (show RAB5A Antibodies) to Rab7.
WDR91 serves as a Rab7 (show RAB7B Antibodies) effector that is essential for neuronal development by facilitating endosome conversion in the endosome-lysosome pathway.
The Vici syndrome protein EPG5 (show EPG5 Antibodies) is a Rab7 (show RAB7B Antibodies) 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 Antibodies) accumulated in GCase (show GBA Antibodies) deficient cells, supporting the notion that lysosomal recycling is impaired. Since recombinant GCase (show GBA Antibodies) can reverse ALR (show GFER Antibodies) impairment, we anticipate that strategies to restore GCase (show GBA Antibodies) activity in the brains of both sporadic patients with PD and those with GBA1 (show GBA Antibodies) 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 Antibodies) filaments facing the wound, indicating that Rab7a has a role in the orientation of vimentin (show VIM Antibodies) filaments during migration
The study highlighted the importance of a phosphorylation/dephosphorylation switch in controlling timely Rab7 (show RAB7B Antibodies) localization and activity on endosomes.
show that the maturation of Mtb (show NCAPG2 Antibodies)-containing autophagosomes into autolysosomes required recruitment of the late endosome marker RAB7 (show RAB7B Antibodies), forming the intermediate compartment amphisomes
We validated ANKRD13A as a novel constituent of BCR (show BCR Antibodies) signalosome and showed that BCR (show BCR Antibodies)-induced phosphorylation of RAB7A at S72 regulates its association with its effector proteins and with endo-lysosomal compartments.
Hepatitis B virus can regulate its own secretion through an activation of the endo-lysosomal and autophagic pathway mediated by Rab7 (show RAB7B Antibodies) activation.
provides molecular insights into the essential role of Vps26 (show VPS26A Antibodies) and Vps35 (show vps35 Antibodies) in Rab7 (show RAB7B Antibodies)-mediated recruitment of the core retromer complex
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.
ras-related protein Rab-7
, ras-related protein Rab-7a
, RAB7A, member RAS oncogene family
, rab7A protein
, ras-related protein rab-7a
, RAB7, member RAS oncogene family
, dystrophin-associated glycoprotein 1
, Ras-associated protein RAB7
, GTP-binding protein (rab7)
, ras-related protein BRL-RAS
, ras-related protein p23