Ask about this productRelated genes to: IFRD1 antibody
- Gene:
- IFRD1 NIH gene
- Name:
- interferon related developmental regulator 1
- Previous symbol:
- -
- Synonyms:
- PC4, TIS7
- Chromosome:
- 7q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-01-21
- Date modifiied:
- 2016-02-03
Related products to: IFRD1 antibody
Related articles to: IFRD1 antibody
- The ability of epithelial cells to cope with injury and undergo regeneration depends on tightly coordinated cellular responses. IFRD1 is a stress-responsive protein that is evolutionarily conserved and required for the cellular regeneration program paligenosis; however, how IFRD1 works in paligenosis is not known. Here we demonstrate that IFRD1 is primarily a cytosolic ribosome-binding protein, specifically binding 80S monosomes that are not actively engaged in translation. Using multiple in vivo and in vitro injury models, including cerulein-induced pancreatitis in mice and tunicamycin-induced ER stress in cell culture, we demonstrate that IFRD1 acts as a ribosome-salvaging factor, preventing ribosomes from degradation. In the absence of IFRD1 during ER stress, non-translating 80S ribosomes were unstable and prone to disassembly and selective degradation. The resulting accumulation of degraded ribosomal subunits overwhelmed cellular autophagic machinery, as evidenced by accumulation of the autophagy-tagging protein p62, even though overall autophagic flux remained unaffected. Ultimately, cells lacking IFRD1 showed reduced mTORC1 activity followed by increased cell death, consistent with patterns observed in cells lacking IFRD1 during paligenosis. Thus, we detail a previously unrecognized cellular function for IFRD1 in stabilizing and preserving the mature ribosome pool during metabolic and translational transitions such as paligenosis. - Source: PubMed
Publication date: 2026/05/07
Cho Charles JCrowder Molly KRougeau Amala KNguyen ThanhBark Steven JLee SammyBrown Jeffrey WMills Jason C - - Source: PubMed
Publication date: 2026/04/28
Lanthier NicolasStärkel PeterSpahr Laurent - The mechanisms underlying metabolic remodeling in metabolic dysfunction-associated steatotic liver disease (MASLD) remain unclear. Targeting the process of de novo lipogenesis (DNL) in the liver has the potential to mitigate MASLD. Here we show that interferon-related developmental regulator 1 (IFRD1) expression negatively correlates with MASLD/metabolic-associated steatohepatitis (MASH) progression in human liver tissues. In multiple mouse models, Ifrd1 mice exhibit an exacerbated MASLD phenotype, while hepatocyte-specific IFRD1 expression suppresses MASH progression. Mechanistically, IFRD1 promotes GLUD1's mitochondrial localization via direct interaction, stabilizing the enzyme's activity to enhance α-ketoglutarate (α-KG) production. α-KG reduces H3K36me3 level at lipogenic genes, thereby inhibiting DNL and ameliorating MASH. α-KG supplementation reverses MASH exacerbation in Ifrd1-CKO mice. Collectively, our research establishes the IFRD1-GLUD1-α-KG axis as a critical metabolic-epigenetic regulatory hub, providing novel targets for inhibiting hepatic DNL and developing therapeutic agents for MASLD/MASH. - Source: PubMed
Publication date: 2026/04/06
Geng MengyaMeng FanzhengLi HairuiSun LijieSun XuedanDing YuShi RongdongqingWang ZhihuaHuang YabinWang JizhouLiu YaoWang JiabeiLittle Peter JXu SuowenLiu LianxinWeng JianpingLuo Sihui - Liver regeneration is a tightly regulated process requiring coordinated interactions between hepatocytes and non-parenchymal cells; however, its molecular mechanisms remain incompletely defined. Here, we aimed to investigate the role of interferon-related developmental regulator 1 (IFRD1) in regulating metabolic-immune crosstalk during liver regeneration. - Source: PubMed
Publication date: 2026/03/18
Zeng TaofeiHuang YabinHe HaoChang JiuxiangTao ShengweiLiu ZihaoThorne Rick FrancisChen WeiqiaoLiu KejiaSun XuedanLiu LianxinYin Dalong - Differentiated cells can return to a progenitor-like state in response to injury via the evolutionarily conserved cellular program called paligenosis. Paligenosis proceeds by three stages: 1) autophagy/autodegradation of differentiated cell architecture, 2) metaplasia/progenitor gene induction, 3) TOR complex 1 (TORC1)-dependent cell cycle re-entry. Using multiple injury and reverse-lineage-tracing approaches in the gut, we show that mature polyploid enterocytes dedifferentiate into diploid progenitors in response to epithelial injury. Several key findings suggest a role for paligenosis. Shortly after injury, enterocytes dramatically increased autophagic flux (stage 1); additionally, pharmacological and genetic inhibition of autophagy blocked progenitor recruitment. Rapamycin also blocked recruitment, indicating that TORC1 is required (stage 3). Finally, RNAi knockdown of , an evolutionarily conserved protein required for paligenosis, blocked progenitor recruitment. Thus, replenishment of diploid progenitors from differentiated polyploid cells may occur by paligenosis. The gut may offer a versatile system for dissecting the mechanisms of this evolutionarily conserved pathway. - Source: PubMed
Publication date: 2026/02/16
Park DongkookLawrence Robert MJackson TylerLi HongjieMills Jason C