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upon phosphorylation of Sara, endosomes detach from the spindle during pIIa targeting.
Notch binds Uninflatable, and both traffic together through Sara endosomes, which is essential to direct asymmetric endosomes motility and Notch-dependent cell fate assignation.
Sara itself contributes to the control of the intestinal stem cells asymmetric division.
PP1 binds Sara and negatively regulates Dpp signaling in Drosophila melanogaster.
During mitosis, Sara endosomes associate with the spindle machinery to segregate into the two daughter cells, daughter cells thereby inherited equal amounts of signaling molecules and retained the Dpp signaling levels of the mother cell
asymmetric targeting of Delta and Notch-containing Sara endosomes will increase Notch signalling in sensory organ precursor daughter cell, pIIa, and decrease it in pIIb
This study describes the expression of two SARA isoforms, SARA1 and SARA2, in mice and reports the generation and characterization of SARA mutant mice with FYVE domain deletion. The loss of SARA promoted skin tumor formation and malignant progression.
osteoblast targeted expression of a mutant endofin protein lacking the pp1c binding activity results in sustained signaling of the BMP type I receptor, which increases bone formation and skeletal angiogenesis.
SARA expression was significantly upregulated in the temporal cortex of patients with temporal lobe epilepsy.
we have identified endofin as an important signalling component required for basal and BMP-induced hepcidin expression.
SARA may serve as a potential novel target in pre-Epithelial-mesenchymal transition states for the amelioration renal fibrosis seen in chronic kidney diseases
PI3K-C2a was also required for TGFb receptor-mediated formation of SARA-Smad2/3 complex
The negative influence that perturbation of RNF11 and SARA levels exerts on the lysosomal degradation of EGFRs could underscore the significance of overexpression of RNF11 in certain cancers.
TGF-beta1 can induce epithelial-to-mesenchymal transition through reduction in SARA expression, SARA is also basally regulated by its interaction with PI3K.
no correlation between SARA expression and the levels of TGF-beta1-induced phosphorylation of Smads in various B-cell lymphomas
SARA binds to ERBIN using a new domain, which we have called the ERBID (ERBIN-binding domain)
After stimulation with glucose, expression of SARA decreased in a time-dependent manner in epithelium to mesenchymal transition of proximal tubule cells.
Expression of a SARA mutant protein lacking the FYVE finger inhibits downstream activin A signaling in endothelial cells.
role in rab5 mediated endocytosis
SARA MH2 domains function in TGF-beta signaling
internalization is important for transforming growth factor beta1-induced Smad2 association with Smad anchor for receptor activation (SARA) and Smad2-dependent signaling in human mesangial cells
SARA acts as a Smad anchor for receptor activation in BMP signaling.
Protein-protein and protein-lipid interactions organized by SARA regulate the vesicular targeting of rhodopsin-bearing axonemal vesicles to nascent discs at the base of the rod outer segment.
SARA has a role in regulating cell phenotype and its effects are mediated through modification of the balance between Smad2 and Smad3 signaling
This gene encodes a double zinc finger motif-containing protein that participates in the transforming growth factor-beta (TGFB) signalling pathway. The encoded protein interacts directly with SMAD2 and SMAD3, and recruits SMAD2 to the TGFB receptor. There are multiple pseudogenes for this gene on chromosomes 2, 15, and X. Alternative splicing results in multiple transcript variants.
, smad anchor for receptor activation
, MAD, mothers against decapentaplegic homolog interacting protein, receptor activation anchor
, zinc finger FYVE domain-containing protein 9
, MADH-interacting protein
, novel serine protease