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Nutrition: Vitamins
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Total 289 results found since Jan 2013.
Vitamin D Receptor Regulates Autophagy to Inhibit Apoptosis and Promote Proliferation in Hepatocyte Injury
CONCLUSIONS: VDR mediates hepatocyte apoptosis and proliferation through autophagy.PMID:36908130 | DOI:10.1272/jnms.JNMS.2023_90-114
Source: Journal of Nippon Medical School - March 13, 2023 Category: Universities & Medical Training Authors: Mingming Fang Chen Zhong Source Type: research
Regulation of XPC Binding Dynamics and Global Nucleotide Excision Repair by p63 and Vitamin D Receptor
J Phys Chem B. 2023 Mar 6. doi: 10.1021/acs.jpcb.2c07257. Online ahead of print.ABSTRACTp63 and the vitamin D receptor (VDR) play important roles in epidermal development and differentiation, but their roles and relationship in the response to ultraviolet (UV) radiation are less clear. Using TERT-immortalized human keratinocytes expressing shRNA targeting p63 in concert with exogenously applied siRNA targeting VDR, we assessed p63 and VDR's separate and combined effect on nucleotide excision repair (NER) of UV-induced 6-4 photoproducts (6-4PP). Knockdown of p63 reduced VDR and XPC expression relative to nontargeting contro...
Source: Health Physics - March 6, 2023 Category: Physics Authors: Christian T Wong Katherine Ona Dennis H Oh Source Type: research
Vitamin D3 alleviates inflammation in ulcerative colitis by activating the VDR-NLRP6 signaling pathway
In this study, we carried out histological and physiological analyses in UC patients and UC mice. RNA sequencing (RNA-seq), assays for transposase-accessible chromatin with high-throughput sequencing (ATAC-seq), chromatin immunoprecipitation (ChIP) assays and protein and mRNA expression were performed to analyze and identify the potential molecular mechanism in UC mice and lipopolysaccharide (LPS)-induced mouse intestinal epithelial cells (MIECs). Moreover, we established nucleotide-binding oligomerization domain (NOD)-like receptor protein nlrp6-/- mice and siRNA-NLRP6 MIECs to further characterize the role of NLRP6 in an...
Source: Frontiers in Immunology - February 8, 2023 Category: Allergy & Immunology Source Type: research
Calcitriol Suppressed Isoproterenol-induced Proliferation of Cardiac Fibroblasts via Integrin β3/FAK/Akt Pathway
ConclusionThese findings revealed a novel role for CAL in suppressing the CFs growth by the downregulation of the integrin β3/FAK/Akt pathway.
Source: Journal of Huazhong University of Science and Technology -- Medical Sciences -- - January 21, 2023 Category: Research Source Type: research
Significance of Oct-4 transcription factor as a pivotal therapeutic target for CD44 < sup > + < /sup > /24 < sup > - < /sup > mammary tumor initiating cells: Aiming at the root of the recurrence
In this study, we have attempted to identify previously unrecognized CSC survival factors that can be used as druggable targets for bCSCs apoptosis regulators isolated from the TNBC line, MDA MB 468. After a thorough literature review, Oct-4 was identified as the most promising marker for its unique abundance in cancer and absence in normal cells and the contribution of Oct-4 to the sustenance of cancer cells. We then validated a very high expression of Oct-4 in the MDA MB 468 bCSCs population using flow-cytometry. The loss of Oct-4 was carried out using small interfering RNA (siRNA)-mediated knockdown in the bCSCs, follow...
Source: Cell Biology International - December 27, 2022 Category: Cytology Authors: Utsav Sen Shanooja Shanavas Apoorva H Nagendra Muhammad Nihad Debajit Chaudhury Hari K Rachamalla Rajkumar Banerjee Sudheer Shenoy P Bipasha Bose Source Type: research
Retinoic Acid Prevents the Neuronal Damage Through the Regulation of Parvalbumin in an Ischemic Stroke Model
In conclusion, retinoic acid contributes to the preservation of neurons from ischemic stroke by controlling parvalbumin expression and apoptosis-related proteins.PMID:36245066 | DOI:10.1007/s11064-022-03769-9
Source: Neurochemical Research - October 16, 2022 Category: Neuroscience Authors: Ju-Bin Kang Dong-Ju Park Phil-Ok Koh Source Type: research
