ArticleInternational journal of biological sciences2016
Caspase-3/7-mediated Cleavage of β2-spectrin is Required for Acetaminophen-induced Liver Damage.
Article in International journal of biological sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 26 citations in OpenAlex.
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- Impaired reciprocal regulation between SIRT6 and TGF-β signaling in fatty liver.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Loss of SPTBN1 Suppresses Autophagy Via SETD7-mediated YAP Methylation in Hepatocellular Carcinoma Initiation and Development.Cellular and molecular gastroenterology and hepatology · 2022Article
- β2-spectrin (SPTBN1) as a therapeutic target for diet-induced liver disease and preventing cancer development.Science translational medicine · 2021Article
- β2SP/TET2 complex regulates gene 5hmC modification after cerebral ischemia.Journal of cellular and molecular medicine · 2021Article
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- Identification of the fatty acid synthase interaction network via iTRAQ-based proteomics indicates the potential molecular mechanisms of liver cancer metastasis.Cancer cell international · 2020Article
- Actin-spectrin scaffold supports open fenestrae in liver sinusoidal endothelial cells.Traffic (Copenhagen, Denmark) · 2019Article
- The role of βII spectrin in cardiac health and disease.Life sciences · 2018Review
- Inhibition of Estrogen Signaling Reduces the Incidence ofInternational journal of biological sciences · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelledThe ubiquitously expressed β2-spectrin (β2SP, SPTBN1) is the most common non-erythrocytic member of the β-spectrin gene family. Loss of β2-spectrin leads to defects in liver development, and its haploinsufficiency spontaneously leads to chronic liver disease and the eventual development of hepatocellular cancer. However, the specific role of β2-spectrin in liver homeostasis remains to be elucidated. Here, we reported that β2-spectrin was cleaved by caspase-3/7 upon treatment with acetaminophen which is the main cause of acute liver injury. Blockage of β2-spectrin cleavage robustly attenuated β2-spectrin-specific functions, including regulation of the cell cycle, apoptosis, and transcription. Cleaved fragments of β2-spectrin were physiologically active, and the N- and C-terminal fragments retained discrete interaction partners and activity in transcriptional regulation and apoptosis, respectively. Cleavage of β2-spectrin facilitated the redistribution of the resulting fragments under conditions of liver damage induced by acetaminophen. In contrast, downregulation of β2-spectrin led to resistance to acetaminophen-induced cytotoxicity, and its insufficiency in the liver promoted suppression of acetaminophen-induced liver damage and enhancement of liver regeneration.
conclusionsβ2-Spectrin, a TGF-β mediator and signaling molecule, is cleaved and activated by caspase-3/7, consequently enhancing apoptosis and transcriptional control to determine cell fate upon liver damage. These findings have extended our knowledge on the spectrum of β2-spectrin functions from a scaffolding protein to a target and transmitter of TGF-β in liver damage.
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