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抗Mouse (Murine) 抗体:
抗Rat (Rattus) 抗体:
Human Polyclonal APBA1 Primary Antibody for 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. in Journal of molecular endocrinology 2007
Human Polyclonal APBA1 Primary Antibody for ELISA, WB - ABIN451592
Jacobs, Williams, Francis: Cyclin-dependent kinase 5, Munc18a and Munc18-interacting protein 1/X11alpha protein up-regulation in Alzheimer's disease. in Neuroscience 2006
Rat (Rattus) Polyclonal APBA1 Primary Antibody for 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. in Neuron 2013
Results indicate that both X11 and X11L (显示 APBA2 抗体) 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 (显示 APP 抗体) to the small GTPase (显示 RACGAP1 抗体)
Expression of Apba1 in the mouse hippocampus is modulated by a sequence variant (B2 SINE indel) in the 3' UTR (显示 UTS2R 抗体) of Comt (catechol-O-methyltransferase (显示 COMT 抗体)).
Our data support a function for both GSK3 and CDK5 (显示 CDK5 抗体) in amyloid precursor protein (显示 APP 抗体) 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 (显示 LEP 抗体) action.
Reports have demonstrated that KIF17 (显示 KIF17 抗体)-Mint1 association was disrupted and transported cargo was released from its microtubule-based transport when Ser (显示 SIGLEC1 抗体) 1029 of KIF17 (显示 KIF17 抗体) was phosphorylated.
X11s associate primarily with APP (显示 APP 抗体) molecules that are outside of DRM (显示 GREM1 抗体), that the dissociation of APP (显示 APP 抗体)-X11/X11L (显示 APBA2 抗体) complexes leads to entry of APP (显示 APP 抗体) into DRM (显示 GREM1 抗体), and that cleavage of uncomplexed APP (显示 APP 抗体) by BACE (显示 BACE 抗体) within DRM (显示 GREM1 抗体)
These results suggest that the three Mint/X11 proteins regulate Abeta (显示 APP 抗体) production by a novel mechanism that may have implications for therapeutic approaches to altering APP (显示 APP 抗体) cleavage in Alzheimer's disease.
Mint1 causes amyloid precursor protein (显示 APP 抗体) accumulation in the trans-Golgi network.
Mints are necessary for activity-induced APP (显示 APP 抗体) and PS1 (显示 PSEN1 抗体) trafficking and provide insight into the cellular fate of APP (显示 APP 抗体) in endocytic pathways essential for Abeta (显示 APP 抗体) production.
an autoinhibitory mechanism in Mint1 is important for regulating APP (显示 APP 抗体) processing and may provide novel therapies for Alzheimer's disease
Transcriptional co-activators Taz (显示 TAZ 抗体) and Yap (显示 YAP1 抗体) mediate signaling via the amyloid beta protein precursor paralogues APLP1 (显示 APLP1 抗体) and APLP2 (显示 APLP2 抗体) through interactions with Mint1 and Mint3 (显示 APBA3 抗体).
Study identified the conserved binding site for the peptide on the CASK (显示 CASK 抗体) 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 (显示 CALR 抗体) cases compared with controls.
ApoEr2 (显示 LRP8 抗体) regulates cell movement, and both X11alpha and Reelin (显示 RELN 抗体) enhance this effect.
A novel consensus sequence for interaction with the PDZ (显示 INADL 抗体)-1 and PDZ (显示 INADL 抗体)-2 domains of amyloid precursor protein (APP (显示 APP 抗体))-interacting proteins Mint1, Mint2 (显示 APBA2 抗体), and Mint3 (显示 APBA3 抗体) 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