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anti-Mouse (Murine) ANK2 Antibodies:
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Mammalian Monoclonal ANK2 Primary Antibody for 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 for 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 for 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 (show SLC2A4 Antibodies) 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 (show CA2 Antibodies)+) sparks and waves in AnkB (show ANKH Antibodies)(+/-) hearts is due to enhanced CaMKII (show CAMK2G Antibodies)-mediated RyR (show RYR1 Antibodies) phosphorylation, which is caused by higher junctional [Ca(2 (show CA2 Antibodies)+)] and consequent local CaMKII (show CAMK2G Antibodies) 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 (show ANKH Antibodies) is required for Prx (show PRX Antibodies) 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 (show INS Antibodies) resistance
Functional relationships between PIK3C3 (show PIK3C3 Antibodies), dynactin (show DCTN1 Antibodies), and AnkB (show ANKH Antibodies) promote axonal transport of organelles and are required for normal axon length.
These findings identify an interaction between ankyrin-B and both Cav2.1 (show CACNA1A Antibodies) and Cav2.2 (show CACNA1B Antibodies) at the amino acid level that is necessary for proper Cav2.1 (show CACNA1A Antibodies) and Cav2.2 (show CACNA1B Antibodies) targeting in vivo.
Ankyrin-B protein (show LEPREL2 Antibodies) in heart failure: identification of a new component of metazoan cardioprotection.
AnkB (show ANKH Antibodies) reduction alters cardiac Na and Ca transport and enhances the coupled RyR (show RYR1 Antibodies) 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 (show ANK Antibodies) 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 (show CAV1 Antibodies) Interaction Sites Alters Na(+),K(+)-ATPase (show ATP1A1 Antibodies) 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 (show ANK1 Antibodies) repeats in complex with an inhibitory segment from the C-terminal regulatory domain and with a sodium channel Nav1.2 (show SCN2A Antibodies) 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