Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10327812 | PMC |
| http://dx.doi.org/10.18632/oncotarget.28472 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
WNT4 promotes the symmetric fission of crypt in radiation-induced intestinal epithelial regeneration.
Cell Mol Biol Lett
December 2024
Guangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Diseases, Guangdong Institute of Gastroenterology, The Sixth Affiliated Hospital, Sun Yat-Sen University, Guangzhou, People's Republic of China.
Background: Radiotherapy for pelvic malignant tumors inevitably causes intestinal tissue damage. The regeneration of intestinal epithelium after radiation injury relies mainly on crypt fission. However, little is known about the regulatory mechanisms of crypt fission events.
View Article and Find Full Text PDFA Phase 1b study of the OxPhos inhibitor ME-344 with bevacizumab in refractory metastatic colorectal cancer.
Invest New Drugs
December 2024
Division of Oncology, Rutgers Cancer Institute of New Jersey, New Brunswick, NJ, USA.
Antiangiogenic drugs may cause vascular normalization and correct hypoxia in tumors, shifting cells to mitochondrial respiration as the primary source of energy. In turn, the addition of an inhibitor of mitochondrial respiration to antiangiogenic therapy holds potential to induce synthetic lethality. This study evaluated the mitochondrial inhibitor ME-344 in combination with bevacizumab in patients with refractory metastatic colorectal cancer (mCRC).
View Article and Find Full Text PDFFragile X Syndrome (FXS) is characterized by intellectual impairment caused by CGG repeat expansion in the FMR1 gene. When repeats exceed 200, they induce DNA methylation of the promoter and the repeat region, resulting in transcriptional silencing of the FMR1 gene and the subsequent loss of FMRP protein. In the past decade or so, research has focused on the role of FMRP as an RNA-binding protein involved in translation inhibition in the brain in FXS model mice, particularly by slowing or stalling ribosome translocation on mRNA.
View Article and Find Full Text PDFCorrection: AIM2 Deficiency Alleviates Cardiac Inflammation and Hypertrophy in HFD/STZ-Induced Diabetic Mice by Inhibiting the NLRC4/IRF1 Signaling Pathway.
J Cardiovasc Transl Res
December 2024
Department of Endocrinology and Metabolism, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Wu Jin Rd, Hong Kou District, Shanghai, 200032, China.
TAT-1, a phosphatidylserine flippase, affects molting and regulates membrane trafficking in the epidermis of C. elegans.
Genetics
December 2024
Department of Molecular Biology, College of Agriculture, Life Sciences and Natural Resources, University of Wyoming, Laramie, Wyoming 82071.
Membrane trafficking is a conserved process required for import, export, movement, and distribution of proteins and other macromolecules within cells. The Caenorhabditis elegans NIMA-related kinases NEKL-2 (human NEK8/9) and NEKL-3 (human NEK6/7) are conserved regulators of membrane trafficking and are required for the completion of molting. Using a genetic approach we identified reduction-of-function mutations in tat-1 that suppress nekl-associated molting defects.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!