ArticleHistochemistry and cell biology2012
CCDC134 interacts with hADA2a and functions as a regulator of hADA2a in acetyltransferase activity, DNA damage-induced apoptosis and cell cycle arrest.
Article in Histochemistry and cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
- ER-resident CCDC134 safeguards TLR4 maturation by maintaining gp96 stability.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- CCDC134 enhances ovarian reserve function and angiogenesis by directly interacting with INHA in a mouse model of premature ovarian insufficiency.Apoptosis : an international journal on programmed cell death · 2025Article
- CCDC134 controls TLR biogenesis through the ER chaperone Gp96.The Journal of experimental medicine · 2025Article
- Regulated N-glycosylation controls chaperone function and receptor trafficking.Science (New York, N.Y.) · 2024Article
- Further screening of SNP loci of eggshell translucency related genes and evaluation of genetic effects.Poultry science · 2024Article
- CCDC134 facilitates T cell activation through the regulation of early T cell receptor signaling.Frontiers in immunology · 2023Article
- Navigating the genomic instability mine field of osteosarcoma to better understand implications of non-coding RNAs.Biocell : official journal of the Sociedades Latinoamericanas de Microscopia Electronica ... et. al · 2022Article
- CCDC134 as a Prognostic-Related Biomarker in Breast Cancer Correlating With Immune Infiltrates.Frontiers in oncology · 2022Article
- α-Synuclein A53T Binds to Transcriptional Adapter 2-Alpha and Blocks Histone H3 Acetylation.International journal of molecular sciences · 2021Article
- Circular RNA circTADA2A promotes osteosarcoma progression and metastasis by sponging miR-203a-3p and regulating CREB3 expression.Molecular cancer · 2019Article
- CCDC134 serves a crucial role in embryonic development.International journal of molecular medicine · 2018Article
- A novel nuclear complex of DRR1, F-actin and COMMD1 involved in NF-κB degradation and cell growth suppression in neuroblastoma.Oncogene · 2017Article
- Combined comparative genomic hybridization and transcriptomic analyses of ovarian granulosa cell tumors point to novel candidate driver genes.BMC cancer · 2015Article
- The Histochemistry and Cell Biology compendium: a review of 2012.Histochemistry and cell biology · 2013Review
- Chemokine-like factor 1 (CLFK1) is over-expressed in patients with atopic dermatitis.International journal of biological sciences · 2013Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human transcriptional adaptor hADA2a is an important component of the general control nonderepressible 5 (GCN5) histone acetyltransferase complex. Here, we report that coiled-coil domain containing 134 (CCDC134), a novel nuclear protein, binds to hADA2a and enhances the stability of the hADA2a protein in unstressed conditions. Furthermore, CCDC134 was found to participate in the p300/CBP-associated factor (PCAF) complex via hADA2a and affect the histone acetyltransferase activity of the complex. We also found that CCDC134 increased the PCAF-dependent K320 acetylation of p53 and p53 protein stability in the presence of hADA2a overexpression. Moreover, we demonstrated the biological significance of the interaction between CCDC134 and hADA2a. CCDC134 showed obvious nuclear accumulation after ultraviolet (UV) irradiation, and the knockdown of endogenous CCDC134 suppressed hADA2a-induced cell apoptosis activity and G1/S cell cycle arrest. Together, our findings indicate that CCDC134 might act as a novel regulator of hADA2a, and plays roles in the PCAF complex via hADA2a to affect its acetyltransferase activity and UV-induced DNA damage repair.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.