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Regulates autophagy and development of the nervous system. Zusätzlich bieten wir Ihnen AMBRA1 Antikörper (112) und AMBRA1 Proteine (3) und viele weitere Produktgruppen zu diesem Protein an.
Ambra1 knockdown causes severe embryonic malformations.
Ambra1 binds to both FAK (zeige PTK2 ELISA Kits) and Src (zeige SRC ELISA Kits) in cancer cells. When FAK (zeige PTK2 ELISA Kits) is present, Ambra1 is recruited to focal adhesions, promoting FAK (zeige PTK2 ELISA Kits)-regulated cancer cell direction-sensing and invasion. However, when Ambra1 cannot bind to FAK (zeige PTK2 ELISA Kits), abnormally high levels of phospho-Src (zeige SRC ELISA Kits) and phospho-FAK (zeige PTK2 ELISA Kits) accumulate at focal adhesions, positively regulating adhesion and invasive migration.
The results suggested that AMBRA1 is a core factor that controls both autophagy and metabolic regulation.
we further measured the expression of autophagy protein BECLIN1 (zeige BECN1 ELISA Kits) in hippocampus of all mice
a de-regulation of c-Myc (zeige MYC ELISA Kits) correlates with increased tumorigenesis in AMBRA1-defective systems, thus supporting a role for AMBRA1 as a haploinsufficient tumour suppressor gene.
found Smad2 (zeige SMAD2 ELISA Kits) as the major transcriptional regulator of autophagy that targets beclin1 (BECN1 (zeige BECN1 ELISA Kits)) gene expression. Smad2 (zeige SMAD2 ELISA Kits), but not Smad3 (zeige SMAD3 ELISA Kits), acts as a repressor upstream of the BECN1 (zeige BECN1 ELISA Kits) promoter region
AMBRA1 interacts with cullin E3 ubiquitin ligases to regulate autophagy dynamics
These results reveal new roles for autophagy-related molecules Atg5 (zeige ATG5 ELISA Kits) and Ambra1 during early neuronal differentiation of stem/progenitor cells.
These data identify interaction of Parkin (zeige PARK2 ELISA Kits) with Ambra1 as a key mechanism for induction of the final clearance step of Parkin (zeige PARK2 ELISA Kits)-mediated mitophagy.
Ambra1 functional deficiency in mouse embryos leads to severe neural tube defects associated with autophagy impairment, accumulation of ubiquitinated proteins, unbalanced cell proliferation and excessive apoptotic cell death
These data suggest a new and interesting role of MIR7-3HG as an anti-autophagic MIRNA that may affect oncogenesis through the regulation of the tumor suppressor AMBRA1.
Results show that the expression of AMBRA1 and Beclin-1 (zeige BECN1 ELISA Kits) is increased in human gastric adenocarcinoma (GC) tissues. High protein expression of AMBRA1 and Beclin-1 (zeige BECN1 ELISA Kits) is correlated with tumor invasion and is an independent poor prognostic marker in GC patients.
Ambra1 is a crucial regulator of autophagy and apoptosis in ovarian cancer cells subject to cisplatin to maintain the balance between autophagy and apoptosis. Ambra1-targeting inhibition might sensitize ovarian cancer cells to chemotherapy.
An increased expression of AMBRA1 and SQSTM1 (zeige SQSTM1 ELISA Kits).
Ambra1 mRNA translocation to P-bodies and translational suppression correlated with increased cell death.
Both AMBRA1 and BECLIN 1 (zeige BECN1 ELISA Kits) affect c-Myc (zeige MYC ELISA Kits) regulation, but through two different pathways.
Ambra1 is a crucial regulator of autophagy and apoptosis in colorectal cancer cells
A schizophrenia-related risk variant in AMBRA1 (rs11819869) is involved in various aspects of impulsivity, and this involvement occurs on a behavioral as well as an imaging genetics level.
Regulates autophagy and development of the nervous system. Involved in autophagy in controlling protein turnover during neuronal development, and in regulating normal cell survival and proliferation.
autophagy/beclin-1 regulator 1
, activating molecule in BECN1-regulated autophagy protein 1-like
, activating molecule in BECN1-regulated autophagy protein 1
, activating molecule in Beclin1-regulated autophagy
, ischemia related factor NYW-1
, DDB1 and CUL4 associated factor 3
, WD repeat domain 94
, activating molecule in beclin-1-regulated autophagy