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Polyclonal RAB7A Primary Antibody pour WB - ABIN540320
Wu, Wang, Loh, Hong, Song: Structural basis for recruitment of RILP by small GTPase Rab7. dans The EMBO journal 2005
Show all 3 Pubmed References
Human Polyclonal RAB7A Primary Antibody pour IF (p), IHC (p) - ABIN720191
Aboul Naga, Dithmer, Chitadze, Kabelitz, Lucius, Roider, Klettner: Intracellular pathways following uptake of bevacizumab in RPE cells. dans Experimental eye research 2015
Human Polyclonal RAB7A Primary Antibody pour ICC, IF - ABIN4348968
Pera, Larrea, Guardia-Laguarta, Montesinos, Velasco, Agrawal, Xu, Chan, Di Paolo, Mehler, Perumal, Macaluso, Freyberg, Acin-Perez, Enriquez, Schon, Area-Gomez: Increased localization of APP-C99 in mitochondria-associated ER membranes causes mitochondrial dysfunction in Alzheimer disease. dans The EMBO journal 2017
structural and biochemical investigation of the Rab7-ORP1L interaction
Rab7a protein is activated by FLCN protein.
Caspase-1 regulates cellular trafficking via cleavage of the Rab7 adaptor protein RILP in cultured neoplastic epithelial cells has been reported.
control of RAB7 activity is not required for the recycling of retromer-dependent cargoes, but instead enables the correct sorting of the autophagy related transmembrane protein ATG9a and autophagosome formation around damaged mitochondria during Parkin-mediated mitophagy.
The authors demonstrate that RABGEF1, the upstream factor of the endosomal Rab GTPase cascade, is recruited to damaged mitochondria via ubiquitin binding downstream of Parkin. RABGEF1 directs the downstream Rab proteins, RAB5 and RAB7A, to damaged mitochondria, whose associations are further regulated by mitochondrial Rab-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 GTP hydrolysis
This paper identifies a CD44s-interacting small GTPase, Rab7A, and shows that CD44s inhibits Rab7A-mediated EGFR trafficking to lysosomes and subsequent degradation.
results indicate that Rab7 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), which serves to redirect ras-related protein Rab-7 (Rab7)-containing vesicles to a kinesin-dependent trafficking mode promoting virion secretion.
Rab7 GTPase 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 complexes.
The results were indicative that rabies virus N proficiently colocalized with Rab5/EEA1 and Rab7/LAMP1 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 is a substrate of Src kinase, and is tyrosine-phosphorylated by Src, withY183 residue of Rab7 being the optimal phosphorylation site for Src. Further investigations demonstrated that the tyrosine phosphorylation of Rab7 depends on the guanine nucleotide binding activity of Rab7 and the activity of Src kinase.
clear effect of subcutaneous zoledronic acid administration in vivo on the prenylation of Rab1A, Rab5B, Rab7A and Rab14 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 effector that is essential for neuronal development by facilitating endosome conversion in the endosome-lysosome pathway.
The Vici syndrome protein EPG5 is a Rab7 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 accumulated in GCase deficient cells, supporting the notion that lysosomal recycling is impaired. Since recombinant GCase can reverse ALR impairment, we anticipate that strategies to restore GCase activity in the brains of both sporadic patients with PD and those with GBA1 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 filaments facing the wound, indicating that Rab7a has a role in the orientation of vimentin filaments during migration
MON1/CALCIUM CAFFEINE ZINC SENSITIVITY1 (CCZ1)-mediated Rab7 activation was indispensable for vacuolar trafficking of tapetum degradation-related cysteine proteases.
Rab7 deficiency exacerbates the severity of acute pancreatitis by impairing the autophagic and endocytic pathways toward lysosomes.
High Rab7 expression is associated with tumor growth and metastasis.
Vps34 has a previously unknown role in regulating Rab7 activity and late endosomal trafficking.
The up-regulation of Rab11, Rab7, or RILP, but not its truncated form RILP-C33, rescued LAMP2A-defective trafficking in cystinosis, whereas dominant-negative Rab11 or Rab7 impaired LAMP2A trafficking.
The inhibition of autophagosome-lysosome fusion induced by SapM is dependent on the interaction between SapM and Rab7.
Prion 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 expression and class-switching in T-dependent and T-independent antibody responses.
CREG1 deficiency influenced the maturation of lysosomes and reduced the espression of Rab7, which might be involved in CREG1-induced cardiomyocyte autophagy.
Tropheryma whipplei blocks the switch from Rab5 to Rab7.
ADRB2 stimulation has caused a marked increase in the autophagy-targeted lipid droplets (LD) for lysosomal degradation, which is dependent on the LD-associated RAB7.
Loss of rab7 is better tolerated in naive T cells than the loss of atg5.
Rab7 is required for LPS-stimulated lysosome tubulation in macrophages.
Signaling protein ras-related protein rab-7A and septin 8 levels were significantly higher in hippocampus of poor contextual fear conditioning extinguishers.
Rab7a is an interacting partner of cellular prion protein in neuronal cells.
Results suggest that Rab7 may play a role in secretory lysosome movement toward the centrosome by interacting with RILP to recruit the minus-end motor, dynein.
Valproic acid improves defective neurite formation in neuroblastoma cells regardless of which Charcot-Marie-Tooth disease-associated Rab7 mutant protein is expressed, an effect mediated via the c-Jun N-terminal kinase (JNK) signaling pathway.
A novel role is demonstrated for SP-A in modulating endolysosomal trafficking via Rab7b (but not Rab5 nor Rab11) in primary alveolar macrophages, and the biochemical pathways are defined.
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 (early endosomes), Rab11a (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