MUC2 antibody (Prediluted for IHC)
- Known as:
- MUC2 (anti-) (Prediluted Immunohistochemistry)
- Catalog number:
- 75r-1038
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- MUC2 antibody (Prediluted for IHC)
Related genes to: MUC2 antibody (Prediluted for IHC)
- Gene:
- BIRC3 NIH gene
- Name:
- baculoviral IAP repeat containing 3
- Previous symbol:
- API2
- Synonyms:
- cIAP2, hiap-1, MIHC, RNF49, MALT2, c-IAP2
- Chromosome:
- 11q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-10
- Date modifiied:
- 2016-10-05
- Gene:
- GIHCG NIH gene
- Name:
- GIHCG inhibitor of miR-200b/200a/429 expression
- Previous symbol:
- -
- Synonyms:
- lncRNA-GIHCG
- Chromosome:
- 12q14.1
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2018-07-25
- Date modifiied:
- 2019-01-25
- Gene:
- MUC2 NIH gene
- Name:
- mucin 2, oligomeric mucus/gel-forming
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 11p15.5
- Locus Type:
- gene with protein product
- Date approved:
- 1989-02-13
- Date modifiied:
- 2017-08-14
Related products to: MUC2 antibody (Prediluted for IHC)
Related articles to: MUC2 antibody (Prediluted for IHC)
- Intestinal goblet cells (GCs) are specialized epithelial cells essential for forming the protective mucus barrier. Recent research has significantly expanded our understanding of their roles beyond mucus secretion, revealing critical functions in immune regulation and mucosal homeostasis. Dysfunction of these cells is implicated in the pathogenesis of intestinal disorders, particularly inflammatory bowel disease (IBD). - Source: PubMed
Publication date: 2026/04/07
Du NingZhang KunGuo JingYan WenlongXu Lingfen - Bisphenol A (BPA) is an endocrine-disrupting chemical that is widely present in aquatic environments. Much research has confirmed that BPA exerts certain toxic effects on the reproduction and development of aquatic organisms. However, current toxicological studies on the changes in gut microbiota and fatty acid metabolism in aquatic organisms exposed to BPA still need to be further elucidated. In this study, Gobiocypris rarus were exposed to BPA at concentrations of 0, 1, 15, and 225 μg/L for 21 days to investigate changes in intestinal microbiota and fatty acid metabolism. Techniques including histological sectioning, fatty acid analysis, 16S rRNA sequencing, and quantitative real-time polymerase chain reaction (qRT-PCR) were employed. The results indicated that BPA exposure induced intestinal tissue damage in rare minnows. Alcian blue-periodic acid Schiff (AB-PAS) staining revealed that BPA exposure significantly promoted mucin secretion and goblet cell maturation. Furthermore, 16S rRNA sequencing indicated that BPA exposure altered gut microbiota composition, with significant increases in the relative abundances of Legionella, Aurantimicrobium, and Rubellimicrobium, while the relative abundance of Cyanobacteriota decreased significantly. Moreover, PICRUSt2 prediction indicated that BPA could disrupt the biosynthesis of secondary metabolites and metabolic pathways. Subsequently, fatty acid analysis showed that BPA exposure induced dysregulation of intestinal fatty acid metabolism, characterized by a significant increase in the relative abundance of butyric acid and saturated fatty acid (SFA), and a significant decrease in the relative abundance of monounsaturated fatty acid (MUFA). qRT-PCR analysis demonstrated that muc-2 and inflammatory factor (il-6, il-10, tnf-α) expression was significantly upregulated after BPA exposure. In summary, this study demonstrates that BPA exposure may impair intestinal health by disrupting gut microbiota and inducing alterations in fatty acid metabolism, particularly changes in butyric acid, which may affect mucus secretion, thereby providing a theoretical basis for assessing BPA's toxic effects on aquatic organisms. - Source: PubMed
Publication date: 2026/04/15
Wang JunWei ZhengjiaLi XinruiWang ZhengyangXu XinghongZhu Long - The global prevalence of functional constipation has witnessed a marked increase due to the imbalanced dietary pattern. The prebiotic function in vitro and the anti-constipation efficacy of garlic polysaccharides (GP) in loperamide-induced constipated mice were evaluated. During in vitro simulated digestion and fecal fermentation, GP showed digestive resistance properties and enhanced abundance of the probiotic bacteria and . In vivo, GP significantly attenuated intestinal oxidative stress. Moreover, GP treatment dose-dependently ameliorated constipation parameters. Notably, GP restored colonic barrier integrity: GP potently upregulated the mRNA expression of tight junction proteins ZO-1 and occludin in the mechanical barrier and exhibited the most substantial restoration of both MUC2 and MUC4 expression levels in the mucins barrier, as well as reduced pro-inflammatory cytokines of TNF-α, IL-1β, IL-17 and elevated anti-inflammatory IL-10 in the immune barrier. Furthermore, GP regulated VIP-cAMP-PKA-AQP3 signaling pathway, which subsequently promoted intestinal water transport and mucus secretion. GP significantly regulated the gut microbiota-SCFAs axis by lowering the ratio and suppressing the level of pathobiont . GP intervention significantly elevated total SCFAs compared to the MOD group ( < 0.05). These results elucidated GP's multi-target mechanism against functional constipation via antioxidant, barrier-repairing, VIP pathway-regulating, and microbiota-directed SCFAs axis. - Source: PubMed
Publication date: 2026/03/17
Li JingfangMiao JiaxinLi TianyiXie ChanyuanXu WentaoChang ShiminChai Ran - This study aimed to investigate whether Baitouweng Decoction(BTD) exerts pharmacodynamic effects on ulcerative colitis(UC) mice with dampness-heat syndrome in the large intestine by modulating the gut microbiota and its metabolites to inhibit the calcium sensing receptor(CaSR)-G-protein alpha subunit Q/G-protein alpha subunit 11(Gq/11)-mitogen activated protein kinase(MAPK) signaling pathway. In the experiment, mice were divided into the following groups: a normal group, a model group, a Baitouweng Decoction fecal microbiota transplantation(BTD-FMT) group, a normal-FMT group, and a normal-FMT + Akkermansia muciniphila group. Except for the normal group, a UC with dampness-heat syndrome model was established in all mice. The corresponding fecal supernatant or Akkermansia muciniphila was administered on days 9, 11, 13, 15, 17, 19, and 21. Items below were recorded: body weight, diet, dampness-heat syndrome modeling conditions, and disease activity index(DAI) scores. The distribution and fluorescence intensity of fluorescein isothiocyanate(FITC)-Dextran in the gut were detected using a small animal 3D live imaging system. Pathological changes in the colon and tongue tissues were observed using hematoxylin-eosin(HE) staining. The mRNA expression of inflammatory factors and Muc2 in colon tissue was measured by quantitative real-time PCR(qRT-PCR). The expression levels of forkhead box protein p3(Foxp3) and retinoic acid related orphan receptor γt(RORγt) in colon tissue were analyzed by immunohistochemistry. Goblet cell and mucin expression were analyzed by alcian blue-periodic acid-Schiff(AB-PAS) staining. Western blot was employed to detect the expression of Zonula occludens-1(ZO-1), Occludin, Claudin-1, CaSR, G-protein alpha subunit αQ(Gnaq), G-protein alpha subunit 11(Gna11), extracellular signal-regulated kinase 1/2(ERK1/2), c-Jun N-terminal kinase(JNK), mitogen-activated protein kinase p38(p38 MAPK, p38), phosphorylated extracellular signal-regulated kinase 1/2(p-ERK1/2), phosphorylated c-Jun N-terminal kinase(p-JNK), and phosphorylated mitogen-activated protein kinase p38(p-p38 MAPK, p-p38) in colon tissue. The results indicated that compared with the normal group, model mice with dampness-heat syndrome showed significant increases in rectal temperature, water intake, DAI scores, total movement trajectories/distance traveled in the open field test, and dampness-heat syndrome scores. Compared with the model group, BTD-FMT exerted therapeutic effects on UC mice with dampness-heat syndrome, which were evidenced by significantly ameliorated dampness-heat symptoms and tongue tissue pathology, reduced DAI scores, restored colon length, decreased colon histopathological scores, and modulated immune responses. Furthermore, BTD-FMT downregulated the mRNA expression of tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β), and interleukin-6(IL-6) while upregulating interleukin-10(IL-10) and interleukin-4(IL-4) expression. Barrier protein levels were appropriately upregulated, alleviating increased intestinal barrier permeability. Additionally, the expression balance between Foxp3 and RORγt was restored, the goblet cell repair and mucin expression were promoted, and the expression of key proteins in the CaSR-Gq/11-MAPK signaling pathway was suppressed in colon tissue. In terms of therapeutic effect, BTD-FMT was superior to normal-FMT. Supplementation with Akkermansia muciniphila partially mimicked the therapeutic effects of BTD-FMT and achieved a synergistic effect when combined with normal-FMT. In conclusion, BTD exerts anti-inflammatory and intestinal mucosal barrier repair effects in UC mice with dampness-heat syndrome via gut microbiota and metabolite modulation, and the CaSR-Gq/11-MAPK signaling pathway inhibition. Akkermansia muciniphila enhances the effect of normal-FMT. - Source: PubMed
Zheng XueYe Dan-DanWeng Xiao-YaHuang Zhuo-WenLi Yi-HuiZhang Lin-ShengChen Mu-YuanLiu Fei-YangZhu Ji-YeDong Ming-GuoZheng Xue-BaoHuang Xiao-Qi - The intestinal mucus layer is comprised of heavily glycosylated mucins, including mucin 2 (MUC2), that serve as a nutrient source for certain bacterial members of the gut microbiota. Only a subset of gut commensals encode the glycoside hydrolases required to degrade mucin glycans. However, mucin-degrading microbes can release glycans and generate compounds that can cross-fed non-mucin degrading microbes, creating complex microbial networks. While pairwise studies have shown that mucin degradation drives cross-feeding and metabolite exchange, the broader impact of mucins on community structure and metabolic output remains poorly understood. In this study, we sought to identify how a defined microbial consortium of human commensals with varied mucin-degrading capacities responds to MUC2 to shape community composition and metabolic output. A defined consortium of human gut commensals with varied mucin-degrading capacities was cultivated in anaerobic bioreactors in the presence or absence of porcine MUC2. Community composition was assessed, and extracellular metabolites were quantified using targeted and untargeted metabolomic profiling. MUC2 supplementation significantly altered community structure, promoting the expansion of while reducing . MUC2 also reshaped microbial metabolism, decreasing acetate levels while increasing propionate, butyrate, and formate. In addition, MUC2 supplementation altered amino acid utilization and vitamin metabolism and reduced several neuroactive compounds, including glutamate, γ-aminobutyric acid (GABA), and anthranilic acid, while increasing tryptamine levels. These findings demonstrate that mucins exert broad effects on microbial community structure and metabolic output. Collectively, this work highlights the central role of bacterial cross-feeding in shaping gut ecosystem function. - Source: PubMed
Publication date: 2026/01/21
Chard ErinHorvath Adelaide EGrozis Makennado Nascimento Renata RochaBaker Paul R SGorti Santosh Kapil KumarProos RobertHorvath Thomas DEngevik Melinda A