| 2000 |
AZU-1 (TACC2) protein resides predominantly in a detergent-extractable cytoplasmic pool in mammary epithelial cells; reexpression of AZU-1 in tumorigenic T4-2 cells was sufficient to reduce their malignant phenotype both in culture and in vivo, establishing a functional tumor-suppressive role in breast morphogenesis. |
Subcellular fractionation, viral vector-mediated reexpression, 3D culture and xenograft assays |
Molecular biology of the cell |
Medium |
10749935
|
| 2003 |
TACC2 physically interacts with GAS41 and components of the SWI/SNF chromatin remodeling complex, suggesting a role in gene regulation via chromatin remodeling. |
Co-immunoprecipitation / pulldown assays |
Genomics |
Medium |
12620397
|
| 2004 |
TACC2 is phosphorylated during mitosis by the TTK kinase signaling pathway; TTK kinase activity is required for centrosomal localization of TACC2, as expression of a kinase-dead TTK mutant or TTK depletion displaces TACC2 from the centrosome (but not other centrosomal proteins such as γ-tubulin and NuMA), leading to chromosome misalignment/lagging and reduced centrosome separation. |
Pulldown of TACC2 by wild-type vs kinase-dead TTK, immunofluorescence, TTK depletion by siRNA |
FEBS letters |
Medium |
15304323
|
| 2004 |
In TACC2-deficient mouse embryonic fibroblasts, proliferation, cell cycle progression, and centrosome numbers are comparable to wild-type cells, indicating TACC2 is dispensable for normal mouse cell proliferation and centrosome homeostasis, and TACC2 knockout mice develop normally without increased tumor incidence. |
TACC2 knockout mouse model, cell proliferation assays, cell cycle analysis, centrosome counting |
Molecular and cellular biology |
High |
15226440
|
| 2009 |
SV40 large T antigen directly binds TACC2 protein; this interaction induces microtubule dysfunction, disorganized mitotic spindles, slow mitotic progression, and chromosome missegregation. Overexpression of TACC2 suppresses T-antigen-induced microtubule destabilization, demonstrating that TACC2 normally stabilizes microtubules in mitosis. |
Co-immunoprecipitation/direct binding assay, N-terminal deletion mutants of T antigen, immunofluorescence microscopy, TACC2 overexpression rescue |
Journal of cell science |
Medium |
19671663
|
| 2012 |
TACC2 is a direct androgen receptor (AR)-regulated gene; a functional AR-binding site containing two canonical androgen response elements was identified near the TACC2 gene with active histone modification marks. AR knockdown or bicalutamide treatment abolished androgen-dependent TACC2 induction. TACC2 siRNA knockdown reduced cell growth and cell cycle progression in castration-resistant prostate cancer (CRPC) cell models, while TACC2 overexpression accelerated the cell cycle. |
ChIP-cloning, ChIP for histone marks, AR knockdown, pharmacological inhibition (bicalutamide), siRNA knockdown, cell cycle analysis, overexpression, castrated mouse xenograft model |
Molecular endocrinology (Baltimore, Md.) |
High |
22456197
|
| 2016 |
Xenopus TACC2 localizes to microtubule plus ends in front of EB1 and overlapping with TACC1/TACC3, functioning as a +TIP. The C-terminal region (containing the TACC domain) is both necessary and sufficient for plus-end localization and promotion of MT polymerization, while the N-terminal region cannot bind MT plus ends but acts in a dominant-negative manner to reduce polymerization rates. TACC2 promotes MT polymerization in mesenchymal cells but not neuronal growth cones. |
Live imaging of GFP-tagged TACC2 in Xenopus embryonic cells, structure-function analysis with N-terminal and C-terminal deletion constructs, MT polymerization rate measurements |
Molecular biology of the cell |
High |
27559128
|
| 2025 |
TACC2 interacts with components of the NuRD and CoREST co-repressor complexes (MTA1, MBD3, HMG20B) in the cytoplasm. Loss of TACC2 causes nuclear translocation of these co-repressor proteins, leading to functional NuRD/CoREST complex assembly in the nucleus, epigenetic repression of CDKN1A (p21), elevated CDK1/2 activation, and increased sensitivity to CDK inhibitors. |
Co-immunoprecipitation, ChIP, TACC2 knockout mouse model, ESCC organoids, subcellular fractionation, siRNA + CDK inhibitor combination treatment in vivo |
Med (New York, N.Y.) |
High |
39793578
|
| 2025 |
TACC2 interacts with the NuRD/CoREST complex and inhibits its nuclear translocation; in soft tissue sarcoma, TACC2 loss permits nuclear NuRD/CoREST translocation which represses CCL3 and CCL4 chemokine transcription, thereby reducing CD8+ T cell infiltration. TACC2 overexpression synergizes with anti-PD-1 therapy in vivo. |
ChIP, co-immunoprecipitation, TACC2 overexpression mouse models, anti-PD-1 combination treatment in vivo |
Molecular cancer |
Medium |
40442694
|
| 2025 |
The PLEKHA1-TACC2 fusion protein activates the EphA2/AKT/MMP2 signaling pathway and promotes vascular mimicry formation by reducing EphA2 ubiquitylation, with oncogenic activity demonstrated in transgenic ESCC mouse models. |
RNA sequencing for fusion identification, functional assays for vascular mimicry, ubiquitylation assay, transgenic mouse model with Trp53 deletion, EphA2 inhibitor treatment in vivo |
Cell death and differentiation |
Medium |
40615663
|
| 2026 |
SUV39H1 (Suv39h1) directly binds the TACC2 promoter and represses TACC2 transcription by catalyzing H3K9 trimethylation during fibroblast-to-myofibroblast transition. TACC2 depletion normalized the transition despite SUV39H1 deficiency, while TACC2 overexpression suppressed the transition, placing TACC2 downstream of SUV39H1 in cardiac fibrosis regulation. |
CUT&Tag-seq, RNA-seq, TACC2 depletion and overexpression, cardiac fibroblast-specific conditional knockout mouse models (Col1a2-CreERT and PostnMCM), transverse aortic constriction heart failure model |
Cardiovascular research |
High |
41861065
|