The ability of cAMP response-element binding protein (CREB)-binding protein (CBP) to function as a co-activator for a number of transcription factors appears to be mediated by its ability to act as a histone acetyltransferase and through its interaction with a number of other proteins (general transcription factors, histone acetyltransferases, and other co-activators). Here we report that CBP also interacts with a novel ATPase termed Snf2-Related CBP Activator Protein (SRCAP). Consistent with this activity, SRCAP contains the conserved ATPase domain found within members of the Snf2 family. Transfection experiments demonstrate that SRCAP is able to activate transcription when expressed as a Gal-SRCAP chimera and that SRCAP also enhances the ability of CBP to activate transcription. The adenoviral protein E1A was found to disrupt interaction between SRCAP and CBP possibly representing a mechanism for E1A-mediated transcriptional repression.
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http://dx.doi.org/10.1074/jbc.274.23.16370 | DOI Listing |
Adv Sci (Weinh)
January 2025
Department of Gynecology, Women's Hospital of Nanjing Medical University, Nanjing Women and Children's Healthcare Hospital, Nanjing Medical University, Nanjing, 210004, P. R. China.
Although a fraction of functional peptides concealed within long non-coding RNAs (lncRNAs) is identified, it remains unclear whether lncRNA-encoded peptides are involved in the malignancy of cervical cancer (CC). Here, a 92-amino acid peptide is discovered, which is named TUBORF, encoded by lncRNA TUBA3FP and highly expressed in CC tissues. TUBORF inhibits ferroptosis to promote the malignant proliferation of CC cells.
View Article and Find Full Text PDFCell Biol Toxicol
January 2025
Department of Ultrasound, Shengjing Hospital of China Medical University, 110004, Shenyang, Liaoning, China.
Histone acetyltransferases p300 (E1A-associated protein p300) and CBP (CREB binding protein), collectively known as p300/CBP due to shared sequence and functional synergy, catalyze histone H3K27 acetylation and consequently induce gene transcription. p300/CBP over-expression or over-activity activates the transcription of oncogenes, leading to cancer cell growth, resistance to apoptosis, tumor initiation and development. The discovery of small molecule inhibitors targeting p300/CBP histone acetyltransferase activity, bromodomains, dual inhibitors of p300/CBP and BRD4 bromodomains, as well as proteolysis-targeted-chimaera p300/CBP protein degraders, marks significant progress in cancer therapeutics.
View Article and Find Full Text PDFACS Pharmacol Transl Sci
January 2025
School of Pharmaceutical Sciences, Sun Yat-Sen University, Guangzhou 510006, P. R. China.
Idiopathic pulmonary fibrosis (IPF) is a debilitating, incurable, and life-threatening disease that lacks effective therapy. The overexpression of phosphodiesterase 10A (PDE10A) plays a vital role in pulmonary fibrosis (PF). However, the impact of selective PDE10A inhibitors on the tumor growth factor-β (TGF-β)/small mother against decapentaplegic (Smad) signaling pathway remains unclear.
View Article and Find Full Text PDFComp Biochem Physiol Part D Genomics Proteomics
January 2025
School of Fisheries, Ludong University, Yantai 264025, China. Electronic address:
Asymmetric development, in which functional differences occur between left-right symmetrical organs, is widespread in organisms, including fish and mollusks. However, the asymmetry of symmetrical sensory structures in Haliotis discus hannai, a gastropod with a sensitive sensory system, remains unknown. This study analyzed the transcriptomes of three sensory structures (eyestalks, cephalic tentacles, and epipodial tentacles) to explore potential asymmetries in this species.
View Article and Find Full Text PDFAdv Sci (Weinh)
January 2025
State Key Laboratory of Membrane Biology, School of Life Sciences, Peking University, Beijing, 100871, China.
The primary cilia serve as pivotal mediators of environmental signals and play crucial roles in neuronal responses. Disruption of ciliary function has been implicated in neuronal circuit disorders and aberrant neuronal excitability. However, the precise mechanisms remain elusive.
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