Ask about this productRelated genes to: SLC9A8 Blocking Peptide
- Gene:
- SLC9A8 NIH gene
- Name:
- solute carrier family 9 member A8
- Previous symbol:
- -
- Synonyms:
- KIAA0939, NHE8
- Chromosome:
- 20q13.13
- Locus Type:
- gene with protein product
- Date approved:
- 2003-03-28
- Date modifiied:
- 2018-11-19
Related products to: SLC9A8 Blocking Peptide
Related articles to: SLC9A8 Blocking Peptide
- Despite the similarities, Crohn's disease (CD) and ulcerative colitis (UC), the two major subtypes of inflammatory bowel disease (IBD), exhibit distinctions. The increasing burden of IBD necessitates discovering novel diagnostic markers. Considering the importance of distinguishing between CD and UC in selecting therapeutic strategies in clinical settings, this investigation focused on identifying subtype-specific blood biomarkers. - Source: PubMed
Publication date: 2026/05/04
Mokaram Doust Delkhah Arman - Reproductive efficiency is an important component of profitability and sustainability in beef cattle production, particularly in tropical environments where animals are routinely exposed to environmental stressors. This study aimed to identify environmentally sensitive SNPs associated with sexual precocity traits in Nellore cattle and characterize candidate genes and biological pathways regulating sexual precocity under variable environmental conditions. For this purpose, three sexual precocity indicators were analyzed; one in heifers (heifer early calving probability at 30 months, HC30), and two in young males (scrotal circumference at 365 days, SC365; age at puberty, APM). Reaction norm models were integrated with genome-wide association studies (GWASs) to identify genomic regions associated with both genetic potential (intercept) and environmental sensitivity (slope). - Source: PubMed
Publication date: 2026/01/21
da Silva Oliveira EduardaRojas de Oliveira HinayahMacedo Mota Lucio FlavioMulim Henrique AlbertoFerreira Campos Milena AparecidaBarbosa da Silva Neto JoãoBaldi Fernando - Colonoscopy remains the gold standard for diagnosing inflammatory bowel disease (IBD) even though it is an invasive and costly procedure. To enable non-invasive diagnosis, we aimed to identify blood-based transcriptomic biomarkers that specifically distinguish IBD from healthy and inflammatory controls. - Source: PubMed
Publication date: 2025/06/20
Nazari Mohammad Hossein DerakhshanGhorbaninejad MahsaShahrokh ShabnamMeyfour Anna - The gastrointestinal Na/H transporter 8 (NHE8) is downregulated in the mucosa of patients with ulcerative colitis, and its deletion in the murine intestine causes a "colitis-like" phenotype. Since ulcerative colitis is characterized by repeated mucosal injury, we investigated the role of NHE8 in intestinal wound repair, by accessing its effect on intracellular pH (pH) regulation, cell proliferation, and migration. NHE8 expression was downregulated via shRNA lentiviral transduction in HT29MTX cells. The selected clonal cell line (HT29/shNHE8) with ∼80% reduced NHE8 mRNA expression displayed an increased proliferative but reduced migratory rate compared with the mock-transduced cells (HT29/pLKO1). The wound front of the HT29/shNHE8 cells consisted of both migrating and nonmigrating cells, and pH measured in this segment displayed the following values: pH(HT29/pLKO.1) = 7.35, pH(HT29/shNHE8) = 7.27, and pH(HT29/shNHE8) = 7.1. The migrating HT29/shNHE8 cells exhibited a significantly increased NHE activity compared with migrating mock-transfected and nonmigrating cells, which was abolished by pharmacological NHE3 inhibition. NHE3 localized to the wound front of HT29/shNHE8, but not to that of HT29/pLKO.1 cells. Cell flattening and lamellipodia development were observed at the wound front in HT29/pLKO.1 cells, whereas the HT29/shNHE8 cells formed tight actin bundles and retained their apical-basal architecture. RAC1 and Cofilin-1, required for the generation of actin-based membrane protrusions, were absent at the wound front of HT29/shNHE8 cells but were expressed in migrating HT29/pLKO.1 cells, where RAC1 partially colocalized with NHE8. The results show that NHE8 downregulation reduces the pH and leads to enhanced epithelial cell proliferation, but impairs migration likely due to altered actin polymerization. The Na/H exchanger 8 (NHE8) plays an important role in the regulation of intracellular pH cell proliferation, and epithelial sheet migration in HT29MTX intestinal cells. NHE8 knockdown cells lack the ability to dynamically rearrange the actin cytoskeleton at the wound front, resulting in a reduced migration rate. These observations provide insights into the molecular mechanism of the downregulation of this transporter in human ulcerative colitis and its role in epithelial restitution. - Source: PubMed
Publication date: 2025/05/28
Wang JuStock ChristianSalari AzamSeidler Ursula ENikolovska Katerina - Vitamin D (VitD) and Vitamin D receptor () are suggested to play protective roles in the intestinal barrier in ulcerative colitis (UC). However, the underlying mechanisms remain elusive. Evidence demonstrates that Na/H exchanger isoform 8 (NHE8, SLC9A8) is essential in maintaining intestinal homeostasis, regarded as a promising target for UC therapy. Thus, this study aims to investigate the effects of VitD/VDR on NHE8 in intestinal protection. VitD-deficient mice, mice and mice were employed in this study. Colitis mice were established by supplementing DSS-containing water. Caco-2 cells and 3D-enteroids were used for in vitro studies. VDR siRNA (siVDR), VDR over-expression plasmid (pVDR), TNF-α and NF-κb p65 inhibitor QNZ were used for mechanical studies. The expression of interested proteins was detected by multiple techniques. In colitis mice, paricalcitol upregulated NHE8 expression was accompanied by restoring colonic mucosal injury. In VitD-deficient and colitis mice, NHE8 expression was compromised with more serious mucosal damage. Noteworthily, paricalcitol could not prevent intestinal barrier dysfunction and histological destruction in mice. In Caco-2 cells and enteroids, siVDR downregulated NHE8 expression, further promoted TNF-α-induced NHE8 downregulation and stimulated TNF-α-induced NF-κb p65 phosphorylation. Conversely, QNZ blocked TNF-α-induced NHE8 downregulation in the absence or presence of siVDR. Our study indicates depressed NHE8 expression is responsible for VitD-deficient-induced colitis aggravation. These findings provide novel insights into the molecular mechanisms of VitD/VDR in intestine protection in UC. - Source: PubMed
Publication date: 2023/11/19
Guo YaoyuLi YanniTang ZeyaGeng ChongXie XiaoxiSong ShuailingWang ChunhuiLi Xiao