Eur J Biochem
Laboratory of Pharmaceutical Science, Nagoya City University, Japan.
Published: August 1990
A mechanism of mitosis-specific enhancement of histone H3 phosphorylation was analyzed in vitro in terms of nucleosome structure. The incorporation of [32P]phosphate into DNA-bound H3 was approximately 5-7 times higher than in DNA-free H3 using the catalytic subunit of cAMP-dependent protein kinase. The two major N-terminal serine sites, including the mitosis-specific site (Ser10) and Ser28, were extensively phosphorylated in the DNA-bound forms. These phosphorylation patterns were identical to those of nucleosomal H3. In contrast, the H3 in DNA-free octamers was very slightly phosphorylated. The major site of H3 phosphorylation in DNA-free H3 was Thr118 in the C-terminus. Results indicate that DNA-binding is essential for the high level of mitosis-specific H3 phosphorylation, and that the nucleosome structure promotes H3 N-terminal phosphorylation in vitro. It also suggests the possibility that H1 prevents H3 phosphorylation during interphase of the cell cycle.
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http://dx.doi.org/10.1111/j.1432-1033.1990.tb19199.x | DOI Listing |
Stem Cell Res Ther
March 2025
Department of Cell Biology and Anatomy, College of Medicine, National Cheng Kung University, No. 1, University Road, Tainan, 70101, Taiwan.
Background: Microenvironmental alterations induce significant genetic and epigenetic changes in stem cells. Mitochondria, essential for regenerative capabilities, provide the necessary energy for stem cell function. However, the specific roles of histone modifications and mitochondrial dynamics in human adipose-derived stem cells (ASCs) during morphological transformations remain poorly understood.
View Article and Find Full Text PDFJ Neuroinflammation
March 2025
Health Science Center, Ningbo University, Ningbo, Zhejiang, 315211, China.
Neuropathic pain, a debilitating nerve injury-induced condition, remains a significant clinical challenge. This study evaluates the effect of histone deacetylase 6 (HDAC6) inhibition in a spared nerve injury (SNI) mouse model. Systemic administration of the selective HDAC6 inhibitor ACY-1215 (20 mg/kg/day, 14 days), alleviated SNI-induced pain in mice of both sexes.
View Article and Find Full Text PDFSci Signal
March 2025
Cancer Research Program, Hospital del Mar Research Institute, CIBERONC, Hospital del Mar, Doctor Aiguader 88, Barcelona 08003, Spain.
The DNA damage repair kinase ATM is phosphorylated by the NF-κB pathway kinase IKKα, resulting in enhanced DNA damage repair through the nonhomologous end-joining pathway. Thus, inhibition of IKKα enhances the efficacy of cancer therapy based on inducing DNA damage. Here, we found a role for the IKK regulatory subunit NEMO in DNA damage repair mediated by ATM and IKKα.
View Article and Find Full Text PDFJ Exp Clin Cancer Res
March 2025
The State Key Laboratory of Pharmaceutical Biotechnology, Department of Hematology, The Affiliated Drum Tower Hospital of Nanjing University Medical School, China-Australia Institute of Translational Medicine, School of Life Sciences, Nanjing University, Nanjing, 210023, China.
Background: Emerging evidence has revealed that PKM2 has oncogenic functions independent of its canonical pyruvate kinase activity, serving as a protein kinase that regulates gene expression. However, the mechanism by which PKM2, as a histone kinase, regulates the transcription of genes involved in triple-negative breast cancer (TNBC) metastasis remains poorly understood.
Methods: We integrated cellular analysis, including cell viability, proliferation, colony formation, and migration assays; biochemical assays, including protein interaction studies and ChIP; clinical sample analysis; RNA-Seq and CUT&Tag data; and xenograft or mammary-specific gene knockout mouse models, to investigate the epigenetic modulation of TNBC metastasis via NONO-dependent interactions with nuclear PKM2.
Phytomedicine
March 2025
Gansu Provincial Cancer Hospital, Gansu Provincial Institute of Medical Sciences, Lanzhou, 730050,PR China. Electronic address:
Background: Radiotherapy is one of the main treatments for non-small cell lung cancer (NSCLC), and radiosensitivity is a determinant of its efficacy. Therefore, enhancing the radiosensitivity is of great significance to improve the clinical efficacy of non-small cell lung cancer (NSCLC).
Purpose: This study intended to investigate the radiosensitisation effect and mechanism of Guiqi Baizhu decoction (GQBZD) on non-small cell lung cancer (NSCLC) and the role of hypoxia-inducible factor-1 alpha (HIF-1α)/DNA-dependent protein kinase catalytic subunit (DNA-PKcs) axis-mediated DNA non-homologous end joining (NHEJ) repair in NSCLC radiotherapy.
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