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A combination of molecular dynamics simulations and computational docking is used to identify a single high-affinity binding site on five beta-tubulin (show TUBB Proteins) microtubule inhibitors adjacent to the exchangeable GTP (show AK3 Proteins) site on beta-tubulin (show TUBB Proteins).
Results suggest that the axonemal motif sequences of betaI, betaIV and betaV tubulin (show TUBB Proteins) are essential for ciliary function.
These data indicate that phosphorylation of tubulin (show TUBB Proteins) by Cdk1 (show CDK1 Proteins) could be involved in the regulation of microtubule dynamics during mitosis.
The data presented here demonstrate that a heterozygous Tubb2b brdp/+ mutation in mice leads to significant spatial learning and memory reductions and conditioned contextual, but not cued, fear deficits.
study shows TUBB2B significantly upregulated in melanoma multinucleated giant cells, which indicates that it may play an important role in melanoma metastasis.
Study showed that Tubb2b is expressed in Sox2 (show SOX2 Proteins)- and Tbr2 (show EOMES Proteins)-positive neuronal progenitors and, at higher levels, in Dcx (show DCX Proteins)-positive postmitotic neurons in the developing mouse neocortex
Results show that the missense mutation at a highly conserved residue (N247S) in Tubb2b gene represents the most severely affected mouse tubulin (show TUBB Proteins) phenotype involving neuronal proliferation and survival.
The TUBB2B mutation described here represents an unusual recessive mode of inheritance for missense-mediated tubulinopathies and reinforces the sensitivity of the developing cerebellum to microtubule defects.
At the cellular level, the p.Cys239Phe TUBB2B mutant leads to tubulin (show TUBB Proteins) heterodimerization impairment, decreased ability to incorporate into the cytoskeleton, microtubule dynamics alteration, with an accelerated rate of depolymerization
off-target, non-immune mediated effects of the mTOR (show FRAP1 Proteins)-inhibitor everolimus on the podocyte cytoskeleton might involve regulation of microtubules, revealing a potential novel role of TUBB2B and DCDC2 (show DCDC2 Proteins) in glomerular podocyte development
The association of polymicrogyria with thin or absent corpus callosum, dysmorphic basal ganglia, brainstem and vermis hypoplasia is highly likely to result from mutations in TUBB2B.
The present study confirms that mutations in tubulin (show TUBB Proteins) genes are responsible for complex brain malformation.
Congenital fibrosis of the extraocular muscles and intellectual disability segregate with a heterozygous mutation in TUBB2B.
The TUBB2B and TUBA1 (show TUBA4A Proteins) coding regions have been sequenced in patients with cortical malformations associated with these genes.
Three new TUBB2B mutations have been identified in three unrelated patients with a diffuse and rather symmetrical cortical abnormality.
Brain malformations are associated with mutations in the beta-tubulin (show TUBB Proteins) gene TUBB2B, supporting its critical role in migration/organization and axon guidance processes.
TUBB2B is required for neuronal migration two disease-associated mutations lead to impaired formation of tubulin (show TUBB Proteins) heterodimers.
The protein encoded by this gene is a beta isoform of tubulin, which binds GTP and is a major component of microtubules. This gene is highly similar to TUBB2A and TUBB2C. Defects in this gene are a cause of asymmetric polymicrogyria.
tubulin beta-2B chain
, tubulin, beta 2A class IIa
, tubulin, beta polypeptide
, beta-tubulin T beta15 (aa 1-445)
, t beta-15
, tubulin, beta 2
, class II beta-tubulin isotype
, class IIb beta-tubulin
, tubulin, beta polypeptide paralog
, neural beta-tubulin
, beta-tubulin class-II
, tubulin beta-2 chain
, tubulin, beta 2B
, hypothetical protein
, tubulin, beta, 2
, tubulin beta-2A chain
, tubulin, beta 2B class IIb