OLFM4 antibody
- Known as:
- OLFM4 (anti-)
- Catalog number:
- orb101702
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- OLFM4 antibody
Related genes to: OLFM4 antibody
- Gene:
- OLFM4 NIH gene
- Name:
- olfactomedin 4
- Previous symbol:
- -
- Synonyms:
- OlfD, GW112, GC1
- Chromosome:
- 13q14.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-06-25
- Date modifiied:
- 2016-10-05
Related products to: OLFM4 antibody
Related articles to: OLFM4 antibody
- Fucosyltransferase 2 (FUT2) deficiency exacerbates inflammation, a known risk factor for colon cancer. However, the precise role and underlying mechanism of FUT2 in regulating colon cancer cell differentiation remain unclear. Although olfactomedin-4 (OLFM4) has been known to have a tumor-suppressive effect, its functional interaction with FUT2 in colon cancer remains unexplored. - Source: PubMed
Duan CaihanZhang KeyiHou LingzhiChen JiaweiLiu JunShi HuiyingHan Chaoqun - Gastric adenocarcinoma (STAD) exhibits extensive intratumoral heterogeneity that contributes to tumor progression and therapeutic resistance. In this study, we integrated single-cell RNA sequencing and bulk transcriptomic analyses to characterize malignant epithelial subtypes in STAD. Among seven identified tumor subtypes, the OLFM4-associated C3 subtype exhibited enriched palmitoylation-related signatures and altered metabolic activities, particularly glycolysis-related pathways. Functional enrichment analyses further supported the enrichment of multiple energy metabolism pathways. To evaluate the association between OLFM4 and metabolic regulation, recombinant OLFM4 treatment and siRNA-mediated OLFM4 knockdown were performed in gastric cancer cell lines. OLFM4 upregulation increased the expression of ZDHHC2 and GLUT1, accompanied by enhanced glucose uptake and elevated ATP production, whereas OLFM4 silencing reduced ZDHHC2 and GLUT1 expression. In addition, a prognostic risk model derived from C3 subtype-associated genes (MUC16, RALA, and PCBD1) effectively stratified STAD patients and was associated with immune checkpoint expression and immune infiltration. Collectively, our findings identify an OLFM4-associated gastric cancer cell state with palmitoylation-related signatures and altered metabolic activities, highlighting its potential relevance to metabolic heterogeneity in gastric adenocarcinoma. - Source: PubMed
Publication date: 2026/06/15
Chen GongWei WeipingLi DanHan ShanshanSchäfer MichaelHuang Xiaoyan - Fasting enhances small intestinal regeneration after radiation, but the contribution of the gut microbiome to this process remains uncharacterized. We identify () as a key mediator of this response. was enriched in fasted mice and its antibiotic depletion abrogated radioprotection, whereas reintroduction restored both organismal survival and intestinal integrity. Fasting elevated propionic acid, consistent with 's metabolic output. -conditioned medium and propionate induced histone H3 acetylation in intestinal stem cell cultures while in vivo fasting induced -dependent H3K27ac and H3K9ac, remodeling promoter-enhancer landscapes in crypt epithelial cells. Epigenetic profiling revealed a rewired core regulatory program enriched for pioneer transcription factors (Foxa, Gata, Klf), architectural organizers (Ctcf, Boris), and lineage-defining and metabolic regulators (Cdx2, Hnf4). This program supports expansion of a population of primed persister cells characterized by open chromatin accessibility at key stem and regenerative-associated loci including , , These findings define a fasting-induced microbiome-metabolite-chromatin axis that epigenetically primes highly plastic persister cells for rapid regeneration of the intestinal epithelium following radiation-induced injury. - Source: PubMed
Publication date: 2026/06/23
Barrodia PraveenSaw Ajay KumarJeter-Jones Sabrina LChang Chia-ChiShao JiansuArslan EmreSingh Anand KSatpati SureshJenq Robert RRai KunalPiwnica-Worms Helen - Ulcerative colitis (UC) is characterized by chronic mucosal inflammation, recurrent epithelial injury, and impaired colonic mucosal wound healing. While WNT/β-catenin dysregulation has been reported in UC, the mechanisms of such abnormalities remain unclear. To investigate epithelial intrinsic alterations associated with UC, we performed single-nucleus RNA-seq (snRNA-seq) and ATAC-seq (snATAC-seq) multiomics on human primary colonic epithelial cells (colonoids) from healthy donors and patients with inactive or active UC. Colonoids were cultured in a 3D matrix recapitulating crypt base cells or grown as 2D monolayers in differentiation medium to recapitulate luminal epithelial cells. Colonoids from active UC had a unique cell population with elevated CTNNB1 and reduced APC expression. Chromatin profiling identified enrichment of RUNX2 motifs in this UC-associated cell population. Active UC colonoids exhibited reduced OLFM4 expression in 3D and the differentiation marker VIL1 in 2D, suggesting impaired epithelial stem-cell maintenance and maturation. RUNX2 inhibition using CADD522 reduced β-catenin levels in 3D colonoids and restored VIL1 expression and junctional β-catenin localization in 2D cultures. These findings reveal an intrinsic defect in epithelial renewal in UC, driven in part by RUNX2-dependent WNT dysregulation. Our study identifies RUNX2 as a transcriptional regulator of epithelial stem cell function and WNT signaling in the inflamed human colon. - Source: PubMed
Publication date: 2026/06/11
Cabrera-Silva Rodolfo IWilson Zachary SMiranda JaelFan ShulingDame MichaelBishu ShrinivasSpence Jason RBrazil Jennifer CColacino JustinNusrat AsmaParkos Charles A - Sepsis is a state of life-threatening organ dysfunction in the setting of infection. It is biologically heterogeneous, as evidenced by whole blood transcriptomic analyses that reveal distinct molecular subtypes based on gene expression. At the cellular level, sepsis is primarily mediated by neutrophils, a leukocyte population increasingly recognized as heterogeneous across several domains. We sought to further characterize neutrophil heterogeneity by identifying neutrophil subsets in critically ill patients with severe sepsis based on multidimensional mass cytometry analysis. - Source: PubMed
Publication date: 2026/06/11
Lima Patricia D AYu ChristinaHunt MirandaLamontagne FrancoisAdhikari Neill K JMarshall John CHindmarch Charles C TMaslove David M