We studied the developmental changes of soluble and membrane-bound protein kinases (EC 2.7.1.37) in rat brain and found that the elution profiles from a DEAE-cellulose column by NaCl of adenosine-3':5'-monophosphate (cyclic AMP) dependent protein kinase from cytosol were not significantly different in newborn (0.19 M NaCl) vs. mature (0.21 M NaCl). In addition, there was little change in Kd for cyclic AMP binding of newborn and mature soluble enzyme. In contrast, using endogenous protein as the phosphate acceptor, cyclic AMP dependent and calcium-dependent protein kinases from brain synaptic membranes of mature rats were significantly higher than that of newborn rats.
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http://dx.doi.org/10.1159/000112450 | DOI Listing |
Clin Epigenetics
January 2025
Faculty of Medicine of TUD Dresden University of Technology, Institute for Clinical Genetics, University Hospital Carl Gustav Carus at TUD Dresden University of Technology, Dresden, Germany.
Autosomal dominant CDK13-related disease is characterized by congenital heart defects, dysmorphic facial features, and intellectual developmental disorder (CHDFIDD). Heterozygous pathogenic variants, particularly missense variants in the kinase domain, have previously been described as disease causing. Using the determination of a methylation pattern and comparison with an established episignature, we reveal the first hypomorphic variant in the kinase domain of CDK13, leading to a never before described autosomal recessive form of CHDFIDD in a boy with characteristic features.
View Article and Find Full Text PDFSignal Transduct Target Ther
January 2025
Division of Molecular Oncology, Centro di Riferimento Oncologico di Aviano (CRO) IRCCS, National Cancer Institute, Aviano, Italy.
Cyclin Dependent Kinases (CDKs) are closely connected to the regulation of cell cycle progression, having been first identified as the kinases able to drive cell division. In reality, the human genome contains 20 different CDKs, which can be divided in at least three different sub-family with different functions, mechanisms of regulation, expression patterns and subcellular localization. Most of these kinases play fundamental roles the normal physiology of eucaryotic cells; therefore, their deregulation is associated with the onset and/or progression of multiple human disease including but not limited to neoplastic and neurodegenerative conditions.
View Article and Find Full Text PDFCancer Biol Ther
December 2025
Department of Hematology, Children's Hospital of Soochow University, Suzhou, China.
Cell cycle dysregulation and the corresponding metabolic reprogramming play significant roles in tumor development and progression. CDK9, a kinase that regulates gene transcription and cell cycle, also induces oncogene transcription and abnormal cell cycle in AML cells. The function of CDK9 for gene regulation in AML cells requires further exploration.
View Article and Find Full Text PDFCell Commun Signal
January 2025
Department of Cell and Molecular Biology, College of Medicine, Chang Gung University, 259 Wen-Hwa 1 road, Guishan District, Taoyuan, Taiwan.
Background: The Golgi apparatus is widely considered a secretory center and a hub for different signaling pathways. Abnormalities in Golgi dynamics can perturb the tumor microenvironment and influence cell migration. Therefore, unraveling the regulatory network of the Golgi and searching for pharmacological targets would facilitate the development of novel anticancer therapies.
View Article and Find Full Text PDFZhongguo Fei Ai Za Zhi
November 2024
Department of Oncology, The Central Hospital of Shaoyang, Shaoyang 422000, China.
With the rapid development of epidermal growth factor receptor (EGFR) gene testing of lung adenocarcinoma patients has been routinely carried out, EGFR mutations are also possible for some small samples of non-smoking female lung squamous cell carcinoma patients. This increases the opportunity for targeted therapy for this group of patients. However, drug resistance in patients with lung squamous cell carcinoma during targeted therapy is an important factor affecting subsequent treatment.
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