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