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Notch (show NOTCH1 ELISA Kits) binds Uninflatable, and both traffic together through Sara endosomes, which is essential to direct asymmetric endosomes motility and Notch (show NOTCH1 ELISA Kits)-dependent cell fate assignation.
Sara itself contributes to the control of the intestinal stem cells asymmetric division.
PP1 binds Sara and negatively regulates Dpp (show TGFb ELISA Kits) 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 (show TGFb ELISA Kits) signaling levels of the mother cell
asymmetric targeting of Delta and Notch (show NOTCH1 ELISA Kits)-containing Sara endosomes will increase Notch (show NOTCH1 ELISA Kits) signalling in sensory organ precursor daughter cell, pIIa, and decrease it in pIIb
This study describes the expression of two SARA (show SAR1A ELISA Kits) isoforms, SARA1 (show SAR1A ELISA Kits) and SARA2 (show SAR1B ELISA Kits), in mice and reports the generation and characterization of SARA (show SAR1A ELISA Kits) mutant mice with FYVE domain deletion. The loss of SARA (show SAR1A ELISA Kits) 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.
we have identified endofin (show ZFYVE16 ELISA Kits) as an important signalling component required for basal and BMP-induced hepcidin (show HAMP ELISA Kits) 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 (show PIK3CA ELISA Kits)-C2a was also required for TGFb (show TGFB1 ELISA Kits) receptor-mediated formation of SARA-Smad2 (show SMAD2 ELISA Kits)/3 complex
The negative influence that perturbation of RNF11 (show RNF11 ELISA Kits) and SARA levels exerts on the lysosomal degradation of EGFRs could underscore the significance of overexpression of RNF11 (show RNF11 ELISA Kits) in certain cancers.
TGF-beta1 (show TGFB1 ELISA Kits) can induce epithelial-to-mesenchymal transition through reduction in SARA expression, SARA is also basally regulated by its interaction with PI3K (show PIK3CA ELISA Kits).
no correlation between SARA expression and the levels of TGF-beta1 (show TGFB1 ELISA Kits)-induced phosphorylation of Smads in various B-cell lymphomas
SARA binds to ERBIN (show ERBB2IP ELISA Kits) using a new domain, which we have called the ERBID (ERBIN (show ERBB2IP ELISA Kits)-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 (show INHBA ELISA Kits) signaling in endothelial cells.
role in rab5 (show RAB5A ELISA Kits) mediated endocytosis
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