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anti-Mouse (Murine) ANK2 Antikörper:
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Mammalian Monoclonal ANK2 Primary Antibody für ISt, IHC - ABIN1304531
Huff, Shi, Sun, Wu, Shi, Cheng: Real-time CARS imaging reveals a calpain-dependent pathway for paranodal myelin retraction during high-frequency stimulation. in PLoS ONE 2011
Show all 9 Pubmed References
Mammalian Monoclonal ANK2 Primary Antibody für ISt, IHC - ABIN1304530
Chang, Zollinger, Susuki, Sherman, Makara, Brophy, Cooper, Bennett, Mohler, Rasband: Glial ankyrins facilitate paranodal axoglial junction assembly. in Nature neuroscience 2014
Show all 6 Pubmed References
Human Monoclonal ANK2 Primary Antibody für FM, ELISA - ABIN967633
Scotland, Zhou, Benveniste, Bennett: Nervous system defects of AnkyrinB (-/-) mice suggest functional overlap between the cell adhesion molecule L1 and 440-kD AnkyrinB in premyelinated axons. in The Journal of cell biology 1999
Show all 5 Pubmed References
Cell-autonomous adiposity results from increased cell surface GLUT4 (zeige SLC2A4 Antikörper) due to ankyrin-B deficiency in humans and mice.
We demonstrate that AnkB binds to Rab GTPase Activating Protein 1-Like (RabGAP1L) and recruits it to PI3P-positive organelles, where RabGAP1L inactivates Rab22A, and promotes polarized trafficking to the leading edge of migrating fibroblasts. We further determine that a5b1-integrin depends on an AnkB/RabGAP1L complex for polarized recycling
The increased incidence of pro-arrhythmogenic Ca(2 (zeige CA2 Antikörper)+) sparks and waves in AnkB (zeige ANKH Antikörper)(+/-) hearts is due to enhanced CaMKII (zeige CAMK2G Antikörper)-mediated RyR (zeige RYR1 Antikörper) phosphorylation, which is caused by higher junctional [Ca(2 (zeige CA2 Antikörper)+)] and consequent local CaMKII (zeige CAMK2G Antikörper) activation.
The identification and characterization of two functionally distinct ankyrin-B isoforms in heart provide compelling evidence that alternative splicing of the ANK2 gene regulates the fidelity of ankyrin-B interactions with proteins
Taken together, these observations reveal that AnkB (zeige ANKH Antikörper) is required for Prx (zeige PRX Antikörper) membrane anchoring and for maintenance of lens fiber cell hexagonal geometry, membrane skeleton organization, and biomechanics.
that ankyrin-B deficiency results in a metabolic syndrome that combines primary pancreatic beta cell insufficiency with peripheral insulin (zeige INS Antikörper) resistance
Functional relationships between PIK3C3 (zeige PIK3C3 Antikörper), dynactin (zeige DCTN1 Antikörper), and AnkB (zeige ANKH Antikörper) promote axonal transport of organelles and are required for normal axon length.
These findings identify an interaction between ankyrin-B and both Cav2.1 (zeige CACNA1A Antikörper) and Cav2.2 (zeige CACNA1B Antikörper) at the amino acid level that is necessary for proper Cav2.1 (zeige CACNA1A Antikörper) and Cav2.2 (zeige CACNA1B Antikörper) targeting in vivo.
Ankyrin-B protein (zeige LEPREL2 Antikörper) in heart failure: identification of a new component of metazoan cardioprotection.
AnkB (zeige ANKH Antikörper) reduction alters cardiac Na and Ca transport and enhances the coupled RyR (zeige RYR1 Antikörper) openings, resulting in more frequent Ca sparks and waves although the total SR Ca leak is unaffected.
The authors discovered that the entire 24 ankyrin (zeige ANK Antikörper) repeats are inhibited by combinatorial and quasi-independent bindings of multiple disordered segments located in the ankyrin-B/G linkers and tails, suggesting a mechanistic basis for differential regulations of membrane target bindings by ankyrins.
we support classification of Ankyrin-B p.L1622I as a "mild" loss-of-function variant that may confer arrhythmia susceptibility in the context of secondary risk factors including environment, medication, and/or additional genetic variation.
Clinical manifestations of ANK2 variants may include QT prolongation and torsades de pointes, often precipitated by strenuous exercise or stress.
Disruption of Ankyrin B and Caveolin-1 (zeige CAV1 Antikörper) Interaction Sites Alters Na(+),K(+)-ATPase (zeige ATP1A1 Antikörper) Membrane Diffusion
Report disease-causing ANK2 variant localized to the membrane-binding domain resulting in reduced ankyrin-B expression and abnormal localization in a First Nations population with a high rate of long QT syndrome.
VariousANK2mutations are associated with a wide range of phenotypes, including aLQTS, especially with ventricular fibrillation, representing "ankyrin-B" syndrome.
Rare Variants in ANK2 Associated With Various Inherited Arrhythmia Syndromes.
the structures of ANK (zeige ANK1 Antikörper) repeats in complex with an inhibitory segment from the C-terminal regulatory domain and with a sodium channel Nav1.2 (zeige SCN2A Antikörper) peptide, are reported.
This gene encodes a member of the ankyrin family of proteins that link the integral membrane proteins to the underlying spectrin-actin cytoskeleton. Ankyrins play key roles in activities such as cell motility, activation, proliferation, contact and the maintenance of specialized membrane domains. Most ankyrins are typically composed of three structural domains: an amino-terminal domain containing multiple ankyrin repeats\; a central region with a highly conserved spectrin binding domain\; and a carboxy-terminal regulatory domain which is the least conserved and subject to variation. The protein encoded by this gene is required for targeting and stability of Na/Ca exchanger 1 in cardiomyocytes. Mutations in this gene cause long QT syndrome 4 and cardiac arrhythmia syndrome. Multiple transcript variants encoding different isoforms have been described.
ankyrin 2, neuronal
, ankyrin repeat and zinc finger domain containing protein 1
, brain ankyrin
, ankyrin B
, ankyrin, brain
, ankyrin-2, nonerythrocytic
, non-erythroid ankyrin
, ankyrin 2, brain
, ankyrin 3, epithelial