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抗Mouse (Murine) TACC3 抗体:
抗Human TACC3 抗体:
抗Rat (Rattus) TACC3 抗体:
Human Polyclonal TACC3 Primary Antibody for IHC, IHC (p) - ABIN4357500
Guo, Partch, Key, Card, Pashkov, Patel, Bruick, Wurdak, Gardner: Regulating the ARNT/TACC3 axis: multiple approaches to manipulating protein/protein interactions with small molecules. in ACS chemical biology 2013
Tacc3 is required for the proper mitosis of Apc-deficient ISCs, and its disruption significantly attenuated the expansion of the crypt domain. In vivo analysis of corresponding mutant mice demonstrated that Tacc3 disruption led to a significant decrease in tumor number and prolonged survival.
Aurora-A kinase does not regulate TACC3-chTOG complex formation, indicating that Aurora-A solely functions as a recruitment factor for the TACC3-chTOG complex to centrosomes and proximal mitotic spindles.
The TACC3 and clathrin were interdependent for spindle recruitment, having to interact in order for either to be recruited to the spindle.
DOCK7 interaction with TACC3 controls interkinetic nuclear migration and the genesis of neurons from radial glial progenitor cells during cortical development
results show that Tacc3 is a vulnerable component of the spindle assembly in lymphoma cells and is a promising cancer chemotherapy target
Tacc3 is a negative regulator of the Notch signaling pathway.
role in hematopoietic stem cell function and interface with p53-regulated apoptosis
REVIEW: genetics, expression, gene expression regulation, and function studies
a role in control the transition between expansion of multipotential progenitor cell populations and final stages of erythroid maturation.
the alpha-helix of FOG-ZF3 recognizes a C-terminal portion of the TACC3 coiled-coil.
in addition to spindle assembly, Tacc3 has critical roles in chromosome separation and cytokinesis, and is essential for the mitosis of sclerotome mesenchymal cells during axial formation in mammals.
HURP recruits TACC3 to regulate K-fiber formation and support chromosome congression.
In vivo evidence for an oncogenic function of FGFR3-TACC3 in respiratory epithelium.
Aurora-A regulates the recruitment of TACC3 to the mitotic spindle through a phospho-dependent interaction with clathrin heavy chain (CHC). Here, we describe the structural basis of these interactions, mediated by three motifs in a disordered region of TACC3.
TACC3 was increased in human RCC cell lines, and knockdown of TACC3 inhibited the ability of cell proliferation, migration, invasion, and tumorigenesis in vivo.
this study suggests that TACC3 might be an important molecular marker for diagnosis and prognosis of breast cancer
Results show that TACC3 region of FGFR3-TACC3 gene fusion can bind and recruit endogenous TACC3 from the spindle. This reduction in TACC3 levels on the mitotic spindle is the primary cause of mitotic defects in urinary bladder.
FGFR3-TACC3 is a recurrent resistance mechanism, which can bypass EGFR blockade by all generations of EGFR TKIs in NSCLC.
TACC3 rs798766 is associated with increased risk of bladder cancer, and no ethnic difference was found.
High levels of TACC3 in human mammary epithelial cells can cause genomic instability possibly in part through destabilizing BRCA1.
TACC3 was highly expressed in CCA tissues and predicted a poor prognosis in CCA patients. TACC3 knockdown induced G2/M cycle arrest and suppressed the invasion, metastasis, and proliferation of CCA cells, both in vitro and in vivo.
Data indicate that transforming acidic coiled-coil protein-3 (TACC3) promotes CRC progression and could be an independent prognostic factor and a potential therapeutic target for colorectal cancer (CRC).
results suggest that TACC3 is an independent prognostic factor and may be a novel therapeutic target for the treatment of ST
The combination treatment of SNIPER(TACC3) and bortezomib exhibited a synergistic anticancer activity in several cancer cell lines.
Study provides evidence of the significant oncogenic potential of the FGFR3-TACC3 fusion protein. The presence of the TACC coiled-coil domain leads to increased and altered levels of FGFR3 activation, fusion protein phosphorylation, downstream signaling, cellular transformation, proliferation, and viability.
Taken together, these findings uncover a supportive role for TACC3 in PCa metastasis, which is mediated by the activation of the Wnt/beta-catenin signaling pathway, suggesting that TACC3 may serve as a prognostic marker in patients with metastatic PCa.
our observations identify TACC3 as an oncogene of tumor malignancy, as well as a prognostic and motoring biomarker for glioma patients.
The results showed that the expression of TACC3 was downregulated in preeclamptic placentas.
TACC3 overexpression was associated with clinicopathological features of aggressiveness, increased EMT-related protein expression, and poor survival, suggesting a potential role for TACC3 as a prognostic biomarker and therapeutic target in HCC
Results showed that high level of TACC3 expression was correlated with advanced clinicopathological classifications, and poor prognosis in non-small cell lung cancer patients indicating that TACC3 is a potential prognostic marker.
TACC3 is enriched in hepatocellular carcinoma and down-regulation inhibits the proliferation, clonogenicity, and cancer stem cell-like phenotype of HCC cells
TACC1 and TACC3 are each required for maintaining normal microtubule growth speed in Xenopus
XTACC3 can induce the recruitment of larger amounts of XMAP215 by increasing its local concentration, thereby promoting efficient microtubule elongation during mitosis
TACC3 promotes axon outgrowth and regulates microtubule dynamics in multiple embryonic cell types.
Results suggest that phosphorylation of maskin by Aurora-A prevents meiosis II proteins from being produced during meiosis I.
Maskin functions in mitotic spindle assembly.
Maskin activity and localization is controlled by differential phosphorylation
Maskin phosphorylation-dephosphorylation also oscillates with the cell cycle and is controlled by the kinase CDK1 and the phosphatase calcineurin
Maskin mRNA is translationally regulated by at least two repressor elements and an activation element.
This gene encodes a member of the transforming acidic colied-coil protein family. The encoded protein is a motor spindle protein that may play a role in stabilization of the mitotic spindle. This protein may also play a role in growth a differentiation of certain cancer cells.
, Arnt interacting protein
, transforming acidic coiled-coil-containing protein 3
, transforming acidic coiled coil 3
, CPEB-associated factor Maskin
, cytoplasmic polyadenylation element-binding protein-associated factor Maskin