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anti-Rat (Rattus) TUBA1A Antibodies:
anti-Human TUBA1A Antibodies:
anti-Mouse (Murine) TUBA1A Antibodies:
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Human Monoclonal TUBA1A Primary Antibody for IF, ELISA - ABIN521658
Niemeyer, Kang, Shin, Furlan, Erlacher, Bunin, Bunda, Finklestein, Sakamoto, Gorr, Mehta, Schmid, Kropshofer, Corbacioglu, Lang, Klein, Schlegel, Heinzmann, Schneider, Starý, van den Heuvel-Eibrink et al.: Germline CBL mutations cause developmental abnormalities and predispose to juvenile myelomonocytic leukemia. ... in Nature genetics 2010
induced pluripotent stem cells (iPSCs) from the umbilical cord and peripheral blood of two lissencephaly patients with different clinical severities carrying alpha tubulin (show TUBA4A Antibodies) (TUBA1A) missense mutations, were generated.
Long intergenic non-coding RNA APOC1P1-3 inhibits apoptosis by decreasing alpha-tubulin (show TUBA4A Antibodies) acetylation in breast cancer.
Results show that Tuba1a plays an essential, noncompensated role in neuronal saltatory migration in vivo and highlight the importance of microtubule flexibility in nucleus-centrosome coupling and neuronal-branching regulation during neuronal migration.
Data show that retinal endothelial cells (HREC) treated with low molecular weight fraction of commercial 5% human serum albumin (show ALB Antibodies) (LMWF5A) exhibit a rapid increase in the amount and distribution of acetylated alpha-tubulin (show TUBA4A Antibodies).
The C-terminal tail from the tubulin beta (show TUBB Antibodies) I isotype, but not the beta III isotype, formed contacts in the putative binding site of a recently discovered antineoplastic peptide that disrupts microtubule formation in glioma cells.
TUBA1B (show TUBA1B Antibodies)/ESR1 (show ESR1 Antibodies) gene interaction might play pivotal roles in the occurrence and development of Postmenopausal Osteoporosis.
data suggest that the TUBA1A mutations disrupting lateral interactions have pronounced dominant-negative effects on microtubule dynamics that are associated with the severe end of the lissencephaly spectrum
Taken together our data provide valuable information regarding the interaction of CK1delta and a-tubulin (show TUBB Antibodies) and a novel approach for the development of pharmacological tools to inhibit proliferation of cancer cells.
Data show that tubulin (show TUBB Antibodies) phosphorylation and acetylation play important roles in the control of microtubule assembly and stability.
Data show that plasma membrane Ca(2+)-ATPase (show ATP2B2 Antibodies) (PMCA) was associated with tubulin (show TUBB Antibodies) in normotensive and hypertensive erythrocytes.
Here the authors demonstrate that mice lacking the alpha-tubulin (show TUBA4A Antibodies) acetyltransferase Atat1 (show C6orf134 Antibodies) in sensory neurons display profound deficits in their ability to detect mechanical stimuli.
Collectively, these findings suggest that Smo and primary cilia-dependent noncanonical Hh signaling leads to post-translational regulation of microtubules and may be important for modulating cell behaviors.
Further PS treatment resulted in recovery of axonal outgrowth and enhanced retrograde axonal transport by decreasing histone deacetylase 6 (HDAC6 (show HDAC6 Antibodies)) levels and thus increasing acetylation of alpha-tubulin (show TUBA4A Antibodies) levels. Thus, we have identified the molecular pathway that leads to neurodegeneration in FD and have demonstrated that phosphatidylserine treatment has the potential to slow progression of neurodegeneration
mass spectrometry-based quantitative comparison of acetylated peptides from wild-type vs HDAC6 (show HDAC6 Antibodies) knockout mice allowed to identify six new deacetylation sites possibly mediated by HDAC6 (show HDAC6 Antibodies).
These results give new insights into the functions of Tuba1a, mechanisms for regulating tubulin (show TUBB Antibodies) proteostasis, and how compromising these may lead to neural defects.
Data indicate that alpha 1a tubulin (show TUBB Antibodies) (Tuba1a) showed the least variability in expression among the different stages of lung development.
Tubulin-tyrosine ligase (TTL (show TTL Antibodies)) is required to increase the levels of tyrosinated alpha-tubulin (show TUBA4A Antibodies) at the axon injury site and plays an important role in injury signaling.
Data suggest a mechanistic link between tubulin (show TUBB Antibodies) hyperacetylation and autophagy induction.
TFIIB (show GTF2B Antibodies) co-localizes and interacts with alpha-tubulin (show TUBA4A Antibodies) during oocyte meiosis in the mouse and depletion of TFIIB (show GTF2B Antibodies) causes arrest of subsequent embryo development.
Acetylation of alpha-tubulin (show TUBA4A Antibodies) is under the control of the acetyltransferase MEC-17 (show C6orf134 Antibodies) and deacetylases SIRT2 (Sirtuin 2 (show SIRT2 Antibodies)) and HDAC6 (histone deacetylase 6 (show HDAC6 Antibodies)). Adipocyte development is inhibited in MEC-17 (show C6orf134 Antibodies)-knockdown cells, but enhanced in MEC-17 (show C6orf134 Antibodies)-overexpressing cells.
TTL (show TTL Antibodies) has specifically evolved to recognize and modify tubulin (show TUBB Antibodies).
LRRK2 (show LRRK2 Antibodies) plays an important role as a physiological regulator for phosphorylation-mediated dissociation of tau from microtubules.
Microtubules of the eukaryotic cytoskeleton perform essential and diverse functions and are composed of a heterodimer of alpha and beta tubulins. The genes encoding these microtubule constituents belong to the tubulin superfamily, which is composed of six distinct families. Genes from the alpha, beta and gamma tubulin families are found in all eukaryotes. The alpha and beta tubulins represent the major components of microtubules, while gamma tubulin plays a critical role in the nucleation of microtubule assembly. There are multiple alpha and beta tubulin genes, which are highly conserved among species. This gene encodes alpha tubulin and is highly similar to the mouse and rat Tuba1 genes. Northern blotting studies have shown that the gene expression is predominantly found in morphologically differentiated neurologic cells. This gene is one of three alpha-tubulin genes in a cluster on chromosome 12q. Mutations in this gene cause lissencephaly type 3 (LIS3) - a neurological condition characterized by microcephaly, mental retardation, and early-onset epilepsy and caused by defective neuronal migration. Alternative splicing results in multiple transcript variants encoding distinct isoforms.
, tubulin alpha-1 chain
, tubulin alpha-1A chain
, tubulin, alpha 1
, tubulin B-alpha-1
, tubulin alpha-3 chain
, tubulin, alpha, brain-specific
, alpha-tubulin 3
, tubulin, alpha 3
, Talpha1 alpha-tubulin
, alpha-tubulin isotype M-alpha-1
, alpha-tubulin ubiquitous
, tubulin K-alpha-1
, tubulin alpha-1B chain
, tubulin alpha-ubiquitous chain
, tubulin, alpha 1a
, tubulin alpha-1A chain-like
, Alpha-tubulin 1
, Tubulin alpha-1 chain
, tubulin alpha 3
, Alpha-tubulin 2
, Alpha-tubulin II
, Tubulin alpha-2 chain
, alpha-tubulin II
, tubulin alpha 1a L homeolog