ArticleBiochemical and biophysical research communications2010
Transforming acidic coiled-coil protein-3 (Tacc3) acts as a negative regulator of Notch signaling through binding to CDC10/Ankyrin repeats.
Article in Biochemical and biophysical research communications, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Centrosome-Signaling Pathway Crosstalk: A Core Hub From Cellular Homeostasis to Disease.Cytoskeleton (Hoboken, N.J.) · 2026Review
- High Expression ofDisease markers · 2022Article
- Inhibiting of TACC3 Promotes Cell Proliferation, Cell Invasion and the EMT Pathway in Breast Cancer.Frontiers in genetics · 2021Article
- Article
- TACC3 transcriptionally upregulates E2F1 to promote cell growth and confer sensitivity to cisplatin in bladder cancer.Cell death & disease · 2018Article
- The ANK repeats of Notch-4/Int3 activate NF-κB canonical pathway in the absence of Rbpj and causes mammary tumorigenesis.Scientific reports · 2017Article
- TACC3 as an independent prognostic marker for solid tumors: a systematic review and meta-analysis.Oncotarget · 2017Article
- TACC3 promotes colorectal cancer tumourigenesis and correlates with poor prognosis.Oncotarget · 2016Article
- TACC3 promotes stemness and is a potential therapeutic target in hepatocellular carcinoma.Oncotarget · 2015Article
- TACC3 deregulates the DNA damage response and confers sensitivity to radiation and PARP inhibition.Oncogene · 2015Article
- Oncogenic FGFR3 gene fusions in bladder cancer.Human molecular genetics · 2013Article
- TACC3 is essential for EGF-mediated EMT in cervical cancer.PloS one · 2013Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
We have identified the transforming acidic coiled-coil protein-3 (Tacc3) as a binding partner for Notch4/Int3 and were able to show that it binds to the intracellular domain (ICD) of all members of the Notch receptor family. Members of the Tacc family reside at the centrosomes and associates with microtubules. Recent studies suggest that Tacc3 also contributes to the regulation of gene transcription. Tacc3 specifically interacts with the Notch4/Int3 CDC10/Ankyrin repeats and to a lesser extent, with residues C-terminal to these repeats in the ICD. Dual label immunofluorescence of mouse mammary tissue shows Tacc3 co-localizes with the Notch3 ICD. Co-immunoprecipitation of endogenous Notch and Tacc3 proteins from NIH3T3 cell extracts, lung and mammary gland confirms that these two proteins interact under physiological conditions. In addition, knock down of Tacc3 in NIH3T3 cells leads to the up-regulation of Hey2, a target gene for Notch signaling. The affinity of Tacc3 binding to Notch4/Int3 ICD is similar to that between Rbpj and Notch4/Int3 ICD. Notch4/Int3 ICD-Tacc3 interaction results in the inhibition of transcription from a Hes1-Luciferase reporter vector in COS-1 cells. The inhibition was reversed in these cells by increasing the levels of Rbpj. Taken together, these results suggest that Tacc3 is a negative regulator of the Notch signaling pathway.
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