Ask about this productRelated genes to: MLXIPL Blocking Peptide
- Gene:
- MLXIPL NIH gene
- Name:
- MLX interacting protein like
- Previous symbol:
- WBSCR14
- Synonyms:
- WS-bHLH, MIO, CHREBP, MONDOB, bHLHd14
- Chromosome:
- 7q11.23
- Locus Type:
- gene with protein product
- Date approved:
- 2000-01-20
- Date modifiied:
- 2016-03-14
Related products to: MLXIPL Blocking Peptide
Related articles to: MLXIPL Blocking Peptide
- Colorectal cancer (CRC) initiating/stem cells (CICs/CSCs) represent a rare tumor subpopulation with self-renewal capacity that drives tumor progression, recurrence, therapeutic resistance, and immune evasion. Despite extensive efforts to define CSCs using surface and functional markers, no universally accepted marker exists for CSC isolation and enrichment. Moreover, the molecular mechanisms underlying CSC-associated phenotypes remain incompletely characterized, highlighting the need for unbiased proteome-wide molecular profiling to better define CSC states and identify candidate biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/04/20
Hussein Ola JTherachiyil LubnaYounis Shahd MItani ShaymaaAbunada Hanan HTout IssamMaccalli CristinaKorashy Hesham M - Diabetic kidney disease (DKD) remains a leading cause of end-stage renal disease despite advances in glucose-, blood pressure-, and albuminuria-lowering therapies. The glucose-responsive transcription factor carbohydrate response element-binding protein (ChREBP; encoded by ) regulates glycolytic-lipogenic programs, yet its causal contribution to renal injury is challenging to disentangle in advanced DKD, where bulk kidney transcriptomes reflect tissue remodeling and cellular compositional shifts. - Source: PubMed
Publication date: 2026/04/15
Liu MingliangChen ShihangWu ShiSun BeiChen Liming - Carbohydrate Response Element Binding Protein (ChREBP) is a transcription factor known to regulate glucose metabolism and other metabolic processes in various tissues, but its role in lung adenocarcinoma (LUAD) remains poorly understood. In this study, we investigated ChREBP expression and its role in regulating gene expression in LUAD cell lines. Using RT-qPCR, we assessed the expression of ChREBP-α and ChREBP-β isoforms in NCI-H1975, NCI-H1650, and NCI-H2228 LUAD cell lines. The NCI-H1975 cells exhibited the highest levels of both ChREBP isoforms, with a particularly pronounced expression of ChREBP-β. To explore the regulatory role of ChREBP, we generated NCI-H1975 cells with inducible expression of a dominant-negative mutant of human ChREBP (dnChREBP). Overexpression of dnChREBP led to a significant reduction in colony formation and impaired cell migration. Transcriptome analysis revealed 57 upregulated genes and 593 downregulated genes in dnChREBP-expressing cells compared to control cells. Functional annotation and gene set enrichment analysis revealed that the enriched genes were associated with cancer-related processes, including cell proliferation and epithelial-to-mesenchymal transition (EMT). Gene network analysis highlighted 17 downregulated hub genes, with 8 of these genes being associated with EMT. Interestingly, ChREBP and its transcriptionally regulated genes, including 4 top downregulated genes, 5 top upregulated genes, and 5 hub genes identified in NCI-H1975 cells overexpressing dnChREBP, showed significant prognostic value, as their expression levels correlated with overall survival in LUAD patients. Our findings suggest that ChREBP regulates distinct transcriptional programs in LUAD cells and ChREBP and its regulatory network may play a potential role in LUAD progression and patient outcomes. - Source: PubMed
Publication date: 2026/04/30
Ruangpracha AthisakeSae-Lee ChanachaiChitta PitaksinGrove HaraldJamjuntra PranisaAmornrit WarisaSuriyaphol PrapatThuwajit ChanitraPoungvarin Naravat - As the most common chronic liver disease, MASLD can progress to metabolic dysfunction-associated steatohepatitis (MASH) driven by accumulated metabolic and inflammatory stresses. We previously reported that liver ChREBPα protein is markedly downregulated in mouse models of diet-induced MASH and hepatotoxin-induced liver injury. Yet the impact of stress pathways on hepatocyte ChREBPα proteolysis has not been examined. Here, we show that a combined metabolic (palmitate, PA) and inflammatory (TNFα) stress signal promotes ubiquitination and proteasome-mediated degradation of ChREBPα in hepatocytes. More importantly, we identify the stress-induced E3 ligase RNF8 as interacting with and promoting ChREBPα ubiquitination and degradation in a JNK2-dependent manner. In vivo, acute depletion of JNK2 or RNF8 stabilizes ChREBPα in mouse liver, increases some but not all ChREBPα transcriptional targets, and reduces diet-induced liver steatosis, inflammation, and fibrosis. Overall, our findings reveal the biochemical machinery underlying stress-induced ChREBPα proteolysis and suggest that targeting RNF8-mediated ChREBPα ubiquitination could be a new strategy for treating MASH. - Source: PubMed
Zhao YueeWang SujuanZhang JianCooke SarahZhang GaryZhao ZifengOh JoonTong XinYin Lei - Mitochondrial dysfunction and the dysregulation of lipid metabolism are significant contributors to vascular aging, which in turn raises the risk of age-related cardiovascular diseases (CVDs). Buyang Huanwu decoction (BHD), a traditional formula widely used for treating CVDs, has not been thoroughly investigated in terms of its active components and the molecular mechanisms by which it may delay vascular aging. - Source: PubMed
Publication date: 2026/04/15
Chen XiangyuChen XiaodieXiao NanYang YutongLi ChenghuiPan YanbinHuang HuiqunDuan XiaodongDeng YonganChen ChengkaiZeng ShutingYang SiminHuang YixuanHuang DanpingYang YubinShu ZunpengZhang Li