Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
Afficher toutes les espèces
Afficher tous les synonymes
Sélectionnez vos espèces et l'application
anti-Rat (Rattus) Anticorps:
anti-Mouse (Murine) Anticorps:
Vous arrivez à notre recherche pré-filtrée.
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
control of RAB7 (Montrer RAB7B Anticorps) activity is not required for the recycling of retromer-dependent cargoes, but instead enables the correct sorting of the autophagy related transmembrane protein ATG9a (Montrer ATG9A Anticorps) and autophagosome formation around damaged mitochondria during Parkin (Montrer PARK2 Anticorps)-mediated mitophagy.
The authors demonstrate that RABGEF1 (Montrer RABGEF1 Anticorps), the upstream factor of the endosomal Rab GTPase (Montrer RAB6A Anticorps) cascade, is recruited to damaged mitochondria via ubiquitin binding downstream of Parkin (Montrer PARK2 Anticorps). RABGEF1 (Montrer RABGEF1 Anticorps) directs the downstream Rab (Montrer HRB Anticorps) proteins, RAB5 (Montrer RAB5A Anticorps) and RAB7A, to damaged mitochondria, whose associations are further regulated by mitochondrial Rab (Montrer HRB Anticorps)-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 (Montrer RAB7B Anticorps) GTP (Montrer AK3 Anticorps) hydrolysis
This paper identifies a CD44s-interacting small GTPase (Montrer RACGAP1 Anticorps), Rab7A, and shows that CD44s inhibits Rab7A-mediated EGFR (Montrer EGFR Anticorps) trafficking to lysosomes and subsequent degradation.
results indicate that Rab7 (Montrer RAB7B Anticorps) 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 (Montrer RILP Anticorps)), which serves to redirect ras-related protein Rab-7 (Rab7 (Montrer RAB7B Anticorps))-containing vesicles to a kinesin-dependent trafficking mode promoting virion secretion.
Rab7 (Montrer RAB7B Anticorps) GTPase (Montrer RACGAP1 Anticorps) 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 (Montrer FRAP1 Anticorps) complexes.
The results were indicative that rabies virus N proficiently colocalized with Rab5 (Montrer RAB5A Anticorps)/EEA1 (Montrer EEA1 Anticorps) and Rab7 (Montrer RAB7B Anticorps)/LAMP1 (Montrer LAMP1 Anticorps) 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 (Montrer RAB7B Anticorps) is a substrate of Src kinase (Montrer CSK Anticorps), and is tyrosine-phosphorylated by Src (Montrer SRC Anticorps), withY183 residue of Rab7 (Montrer RAB7B Anticorps) being the optimal phosphorylation site for Src (Montrer SRC Anticorps). Further investigations demonstrated that the tyrosine phosphorylation of Rab7 (Montrer RAB7B Anticorps) depends on the guanine nucleotide binding activity of Rab7 (Montrer RAB7B Anticorps) and the activity of Src kinase (Montrer CSK Anticorps).
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 (Montrer PIK3C3 Anticorps) has a previously unknown role in regulating Rab7 activity and late endosomal trafficking.
Rab7 accumulated in GCase (Montrer GBA Anticorps) deficient cells, supporting the notion that lysosomal recycling is impaired. Since recombinant GCase (Montrer GBA Anticorps) can reverse ALR (Montrer GFER Anticorps) impairment, we anticipate that strategies to restore GCase (Montrer GBA Anticorps) activity in the brains of both sporadic patients with PD and those with GBA1 (Montrer GBA Anticorps) mutations will improve autophagy lysosomal pathway, preventing the accumulation of a-synuclein and spread of pathology.
The up-regulation of Rab11 (Montrer RAB11A Anticorps), Rab7, or RILP (Montrer RILP Anticorps), but not its truncated form RILP (Montrer RILP Anticorps)-C33 (Montrer CD82 Anticorps), rescued LAMP2A-defective trafficking in cystinosis, whereas dominant-negative Rab11 (Montrer RAB11A Anticorps) or Rab7 impaired LAMP2A trafficking.
The inhibition of autophagosome-lysosome fusion induced by SapM is dependent on the interaction between SapM and Rab7.
Prion (Montrer PRNP Anticorps) 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 (Montrer AICDA Anticorps) expression and class-switching in T-dependent and T-independent antibody responses.
CREG1 (Montrer CREG1 Anticorps) deficiency influenced the maturation of lysosomes and reduced the espression of Rab7, which might be involved in CREG1 (Montrer CREG1 Anticorps)-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 (Montrer Rab5c Anticorps) (early endosomes), Rab11a (Montrer RAB11A Anticorps) (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