The expression of phosphatidylinositol-3 kinase in tumors and homologous tissues from 29 patients with lung cancer, 5 patients with lung metastases of various tumors, and some non-tumorous pulmonary diseases was studied by Western blot analysis. The expression of phosphatidylinositol-3 kinase was increased in these tumors in comparison with histologically intact lung tissue in 5 patients with non-small-cell cancer. In 20 patients expression of phosphatidylinositol-3 kinase was the same as in homologous tissue and in 4 patients it was decreased. No relationship between phosphatidylinositol-3 kinase expression and clinical and morphological characteristics of lung cancer was revealed.
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http://dx.doi.org/10.1007/BF02682016 | DOI Listing |
Anim Cells Syst (Seoul)
January 2025
Department of Biological Sciences and Biotechnology, Chungbuk National University, Cheongju, Republic of Korea.
Osmoregulation is essential for the survival of aquatic organisms, particularly teleost fish facing osmotic challenges in environments characterized by variable salinity. While the gills are known for ion exchange, the intestine's role in water and salt absorption is gaining attention. Here, we investigated the adaptive responses of the intestine to salinity stress in guppies (), observing significant morphological and transcriptomic alterations.
View Article and Find Full Text PDFBiomedica
December 2024
Universidad del Valle, Cali, ColombiaDepartamento de Microbiología, Facultad de Salud, Universidad del Valle, Cali, Colombia; Genetic Immunotherapy Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Disorders, National Institutes of Health, Bethesda, MD, USA.
Activated phosphoinositide 3-kinase δ syndrome is an inborn error of immunity due to mutations within the genes responsible for encoding PI3Kδ subunits. This syndrome results in an excessive activation of the phosphoinositide 3-kinase signaling pathway. Gainof-function mutations in the gene PIK3R1 (encoding p85α, p55α, and p50α) lead to the development of the activated PI3K δ syndrome.
View Article and Find Full Text PDFElife
January 2025
The University of Cambridge Metabolic Research Laboratories, Wellcome Trust-MRC Institute of Metabolic Science, Cambridge, United Kingdom.
encodes three regulatory subunits of class IA phosphoinositide 3-kinase (PI3K), each associating with any of three catalytic subunits, namely p110α, p110β, or p110δ. Constitutional mutations cause diseases with a genotype-phenotype relationship not yet fully explained: heterozygous loss-of-function mutations cause SHORT syndrome, featuring insulin resistance and short stature attributed to reduced p110α function, while heterozygous activating mutations cause immunodeficiency, attributed to p110δ activation and known as APDS2. Surprisingly, APDS2 patients do not show features of p110α hyperactivation, but do commonly have SHORT syndrome-like features, suggesting p110α hypofunction.
View Article and Find Full Text PDFChin Med J Pulm Crit Care Med
December 2024
Department of Respiratory Medicine, National Key Clinical Specialty, Branch of National Clinical Research Center for Respiratory Disease, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China.
Background: Glucocorticoid-induced transcript 1 (GLCCI1) has been reported to be associated with the efficiency of inhaled glucocorticoids in patients with asthma. This study aimed to investigate the role of GLCCI1 in the regulation of nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) family pyrin domain-containing 3 (NLRP3) by the phosphatidylinositol 3-kinase (PI3K) pathway in the pathogenesis of allergic asthma.
Methods: The expression levels of genes encoding GLCCI1, NLRP3 inflammasome components, and PI3K pathway-related indicators were detected in cells isolated from induced sputum from patients with asthma and healthy controls.
Exp Eye Res
January 2025
Department of Ophthalmology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China. Electronic address:
The abrupt and substantial elevation of intraocular pressure (IOP) in acute glaucoma induces retinal ischemia/reperfusion (I/R) injury, resulting in progressive retinal ganglion cell (RGC) death and irreversible visual impairment. PANoptosis, a form of regulated cell death consisting of pyroptosis, apoptosis and necroptosis, is reported to be involved in high IOP-induced RGC death. However, the precise mechanisms of RGC death remain unclear, and neuroinflammation is considered to play a vital role.
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