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Transcriptomic landscape of hyperthyroidism in mice overexpressing thyroid-Stimulating hormone.
iScience
January 2025
Medical Research Institute KITANO HOSPITAL, PIIF Tazuke-kofukai, Kita-ku, Osaka 530-8480, Japan.
Activation of thyroid-stimulating hormone receptor (TSHR) fundamentally leads to hyperthyroidism. To elucidate TSHR signaling, we conducted transcriptome analyses for hyperthyroid mice that we generated by overexpressing TSH. TSH overexpression drastically changed their thyroid transcriptome.
View Article and Find Full Text PDFComputational Analysis Suggests That AsnGTT 3'-tRNA-Derived Fragments Are Potential Biomarkers in Papillary Thyroid Carcinoma.
Int J Mol Sci
October 2024
Research Service, VA San Diego Healthcare System, San Diego, CA 92161, USA.
Transfer-RNA-derived fragments (tRFs) are a novel class of small non-coding RNAs that have been implicated in oncogenesis. tRFs may act as post-transcriptional regulators by recruiting AGO proteins and binding to highly complementary regions of mRNA at seed regions, resulting in the knockdown of the transcript. Therefore, tRFs may be critical to tumorigenesis and warrant investigation as potential biomarkers.
View Article and Find Full Text PDFTranscriptomic Insights into Different Stimulation Intensity of Electroacupuncture in Treating COPD in Rat Models.
J Inflamm Res
May 2024
Acupuncture and Tuina School, Chengdu University of Traditional Chinese Medicine, Chengdu City, Sichuan Province, People's Republic of China.
Background: Electroacupuncture (EA), with varying stimulation intensities, has demonstrated therapeutic potentials in both animal and clinical studies for the treatment of chronic obstructive pulmonary disease (COPD). However, a comprehensive investigation of the intensity-related effects, particularly 1mA and 3mA of EA, and the underlying mechanisms remains lacking.
Methods: A COPD rat model was established by prolonged exposure to cigarette smoke and intermittent intratracheal instillation of lipopolysaccharide.
Angiotensin II acts through Rac1 to upregulate pendrin: role of NADPH oxidase.
Am J Physiol Renal Physiol
February 2024
Renal Division, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, United States.
Article Synopsis
- * Knocking out Rac1 in intercalated cells lowered pendrin levels when these cells were treated with angiotensin II, suggesting Rac1 is important for this increase.
- * The research indicates Rac1 may regulate pendrin by involving NADPH oxidase, affecting oxidative stress and ultimately blood pressure responses in the kidneys treated with angiotensin II.
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