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Human Polyclonal APBA1 Primary Antibody pour ELISA, WB - ABIN1003416
Verlaeten, Casery, Cavagna, Naville, Giraudon, Belin, Begeot, Bernard: Identification of Urop11, a novel leptin-modulated gene that is upregulated in the hypothalamus of mice with virus-induced obesity. dans Journal of molecular endocrinology 2007
Rat (Rattus) Polyclonal APBA1 Primary Antibody pour ICC, IHC - ABIN1742315
Boyken, Grønborg, Riedel, Urlaub, Jahn, Chua: Molecular profiling of synaptic vesicle docking sites reveals novel proteins but few differences between glutamatergic and GABAergic synapses. dans Neuron 2013
Human Polyclonal APBA1 Primary Antibody pour ELISA, WB - ABIN451592
Jacobs, Williams, Francis: Cyclin-dependent kinase 5, Munc18a and Munc18-interacting protein 1/X11alpha protein up-regulation in Alzheimer's disease. dans Neuroscience 2006
Results indicate that both X11 and X11L (Montrer APBA2 Anticorps) exert largely in brain neurons, but X11 may also function in peripheral tissues.
Due to the multiple interacting partners of X11alpha, dysfunction or alteration in X11alpha will have a significant cellular effect.
Mint1 826 bridges APP (Montrer APP Anticorps) to the small GTPase (Montrer RACGAP1 Anticorps)
Expression of Apba1 in the mouse hippocampus is modulated by a sequence variant (B2 SINE indel) in the 3' UTR (Montrer UTS2R Anticorps) of Comt (catechol-O-methyltransferase (Montrer COMT Anticorps)).
Our data support a function for both GSK3 and CDK5 (Montrer CDK5 Anticorps) in amyloid precursor protein (Montrer APP Anticorps) processing, further implicating these two kinases in the pathogenesis of Alzheimer's disease.
Can be considered a key molecule in the hypothalamic integration pathway, important as a target of leptin (Montrer LEP Anticorps) action.
Reports have demonstrated that KIF17 (Montrer KIF17 Anticorps)-Mint1 association was disrupted and transported cargo was released from its microtubule-based transport when Ser (Montrer SIGLEC1 Anticorps) 1029 of KIF17 (Montrer KIF17 Anticorps) was phosphorylated.
X11s associate primarily with APP (Montrer APP Anticorps) molecules that are outside of DRM (Montrer GREM1 Anticorps), that the dissociation of APP (Montrer APP Anticorps)-X11/X11L (Montrer APBA2 Anticorps) complexes leads to entry of APP (Montrer APP Anticorps) into DRM (Montrer GREM1 Anticorps), and that cleavage of uncomplexed APP (Montrer APP Anticorps) by BACE (Montrer BACE Anticorps) within DRM (Montrer GREM1 Anticorps)
These results suggest that the three Mint/X11 proteins regulate Abeta (Montrer APP Anticorps) production by a novel mechanism that may have implications for therapeutic approaches to altering APP (Montrer APP Anticorps) cleavage in Alzheimer's disease.
Mint1 causes amyloid precursor protein (Montrer APP Anticorps) accumulation in the trans-Golgi network.
Mints are necessary for activity-induced APP (Montrer APP Anticorps) and PS1 (Montrer PSEN1 Anticorps) trafficking and provide insight into the cellular fate of APP (Montrer APP Anticorps) in endocytic pathways essential for Abeta (Montrer APP Anticorps) production.
an autoinhibitory mechanism in Mint1 is important for regulating APP (Montrer APP Anticorps) processing and may provide novel therapies for Alzheimer's disease
Transcriptional co-activators Taz (Montrer TAZ Anticorps) and Yap (Montrer YAP1 Anticorps) mediate signaling via the amyloid beta protein precursor paralogues APLP1 (Montrer APLP1 Anticorps) and APLP2 (Montrer APLP2 Anticorps) through interactions with Mint1 and Mint3 (Montrer APBA3 Anticorps).
Study identified the conserved binding site for the peptide on the CASK (Montrer CASK Anticorps) calmodulin kinase domain. A related EPIWVMRQ peptide from Mint1 was also discovered to be sufficient for binding.
Our findings show a new function for X11alpha that may impact on Alzheimer's disease pathogenesis.
Methylation of MINT1 was significantly more prevalent in UC-CRC (Montrer CALR Anticorps) cases compared with controls.
ApoEr2 (Montrer LRP8 Anticorps) regulates cell movement, and both X11alpha and Reelin (Montrer RELN Anticorps) enhance this effect.
A novel consensus sequence for interaction with the PDZ (Montrer INADL Anticorps)-1 and PDZ (Montrer INADL Anticorps)-2 domains of amyloid precursor protein (APP (Montrer APP Anticorps))-interacting proteins Mint1, Mint2 (Montrer APBA2 Anticorps), and Mint3 (Montrer APBA3 Anticorps) is reported, with multiple novel interactors for these proteins.
The protein encoded by this gene is a member of the X11 protein family. It is a neuronal adapter protein that interacts with the Alzheimer's disease amyloid precursor protein (APP). It stabilizes APP and inhibits production of proteolytic APP fragments including the A beta peptide that is deposited in the brains of Alzheimer's disease patients. This gene product is believed to be involved in signal transduction processes. It is also regarded as a putative vesicular trafficking protein in the brain that can form a complex with the potential to couple synaptic vesicle exocytosis to neuronal cell adhesion.
amyloid beta (A4) precursor protein-binding, family A, member 1
, amyloid beta A4 precursor protein-binding, family A, member 1
, amyloid beta (A4) precursor protein-binding, family A, member 1 (X11)
, ketopantoate reductase
, 2-dehydropantoate 2-reductase
, Amyloid beta A4 precursor protein-binding family A member 1
, amyloid beta A4 precursor protein-binding family A member 1-like
, adapter protein X11alpha
, amyloid beta A4 precursor protein-binding family A member 1
, neuron-specific X11 protein
, neuronal Munc18-1-interacting protein 1
, amyloid beta (A4) precursor protein-binding family A APBA1: amyloid beta (A4) precursor protein-binding family A member 1 (X11)
, amyloid beta (A4) precursor protein-binding, family A, APBA1: amyloid beta (A4) precursor protein-binding, family A, member 1 (X11)
, adaptor protein X11alpha
, neuronal munc18-1-interacting protein 1
, phosphotyrosine-binding/-interacting domain (PTB)-bearing protein