2025年1月15日 · NF-κB p65 is known to be a transcriptional activator of S100A16 (Jiang et al., 2021). Here, we validated the binding between p65 and S100A16 in HL-1 cells. We demonstrated that inhibition of VDAC1 decreased p65 activation and consequently suppressed the transcription of S100A16, therefore, alleviating S100A16 expression in cardiac I/R insults.

Importantly, we showed that I/R and H/R treatment upregulated the expression of voltage-dependent anion channel 1 (VDAC1), which subsequently activated NF-κB/p65 to facilitate the binding of NF-κB/p65 to the S100A16 promoter, thereby activating the transcription and expression of S100A16.

2025年1月15日 · Elevated VDAC1 triggered the activation of NF-κB p65, with an upregulated p65 subunit. After translocation to the nucleus, p65 fostered the expression of S100A16, ultimately leading to oxidative stress and inflammatory response via …

2022年12月28日 · As a key protein serving as the mitochondrial gatekeeper, the voltage-dependent anion channel-1 (VDAC1) that controls metabolism and Ca 2+ homeostasis is positioned at a convergence point for various cell survival and death signals.

2018年12月8日 · We demonstrated that silencing VDAC1 expression using human-specific siRNA (si-hVDAC1) inhibited cancer cell growth, both in vitro and in mouse xenograft models of human glioblastoma (U-87MG), lung cancer (A549), and triple negative breast cancer (MDA-MB-231).

VDAC1 functions in the release of apoptotic proteins located in the mitochondrial intermembrane space via oligomerization to form a large channel that allows passage of cytochrome c and AIF and their release to the cytosol, subsequently resulting in apoptotic cell death.

Importantly, we showed that I/R and H/R treatment upregulated the expression of voltage-dependent anion channel 1 (VDAC1), which subsequently activated NF-κB/p65 to facilitate the binding of NF-κB/p65 to the S100A16 promoter, thereby activating the transcription and expression of S100A16.

2024年11月28日 · VDAC1-NF-κB/p65-mediated S100A16 contributes to myocardial ischemia/reperfusion injury by regulating oxidative stress and inflammatory response via …

VDAC1-NF-κB/p65-mediated S100A16 contributes to myocardial ischemia/reperfusion injury by regulating oxidative stress and inflammatory response via Calmodulin/CaMKK2/AMPK pathway.

2024年7月23日 · Voltage-dependent anion channel 1 (VDAC1) is the most abundant protein localized at mitochondrial outer membrane [27], and VDAC1 oligomerization was found to increase the permeabilization of...

2023年12月1日 · VDAC1, the most abundant VDAC isoforms, has been reported to form the large mitochondrial outer membrane pores under mitochondrial stress via oligomers, which are stabilized by mtDNA through direct interaction 26. Therefore, we explored whether VDAC1 could contribute to the release of mtDNA via initiating mPTP opening in ox-LDL-treated HCAECs.

2022年10月10日 · vdac1 调节线粒体 ca 2+运输、脂质代谢和线粒体自噬，参与炎症相关疾病的发病机制。 许多科学家提出了通过特定靶向疗法来处理炎症过度反应问题的方法。

Strikingly, we identified VDAC1 (voltage-dependent anion channel 1) as a target for Parkin-mediated Lys 27 poly-ubiquitylation and mitophagy. Moreover, pathogenic Parkin mutations interfere with distinct steps of mitochondrial translocation, ubiquitylation and/or final clearance through mitophagy.

2025年3月1日 · VDAC1-NF-κB/p65-mediated S100A16 contributes to myocardial ischemia/reperfusion injury by regulating oxidative stress and inflammatory response via …

MedChemExpress (MCE) References: PMID: 39613175 Myocardial injury triggers intense inflammatory reactions and oxidative stress responses. S100 calcium-binding protein A16 (S100A16), a multi-functional calcium (CA2+)-binding protein, participates in inflammatory responses and contributes to ischemia/reperfusion (I/R) injury. Nevertheless, the precise mechanism by which S100A16 operates in ...

2024年7月7日 · In this study, we found that PKC-δ was highly upregulated in human biopsy samples and mouse kidneys with fibrosis. Rottlerin, a PKC-δ inhibitor, alleviated unilateral ureteral ligation...

2022年2月2日 · We have investigated the role of the mitochondria gate-keeper protein, the voltage-dependent-anion channel 1 (VDAC1), in gastrointestinal inflammation and tested the effects of the newly developed VDAC1-interacting molecules, VBIT-4 and VBIT-12, on UC induced by dextran sulfate sodium (DSS) or trinitrobenzene sulphonic acid (TNBS) in mice.

2022年9月28日 · Recently, we developed VDAC1-based peptides that have multiple effects on cancer cells and tumors including apoptosis induction. Here, we designed several cell-penetrating VDAC1 N-terminal-derived peptides with the goal of identifying the shortest peptide with improved cellular stability and activity.

2024年4月16日 · Here, we show that the AAV-mediated upregulation of VDAC1 in the spinal cord of transgenic mice expressing SOD1 G93A completely rescues the mitochondrial respiratory profile.

2024年12月30日 · Voltage-Dependent Anion Channel 1 (VDAC1) is a mitochondrial outer membrane protein that plays a crucial role in regulating cellular energy metabolism and apoptosis by mediating the exchange of ions and metabolites between mitochondria and the cytosol.