Ask about this productRelated genes to: RHBG Blocking Peptide
- Gene:
- RHBG NIH gene
- Name:
- Rh family B glycoprotein (gene/pseudogene)
- Previous symbol:
- -
- Synonyms:
- SLC42A2
- Chromosome:
- 1q22
- Locus Type:
- gene with protein product
- Date approved:
- 2001-05-08
- Date modifiied:
- 2016-01-13
Related products to: RHBG Blocking Peptide
Related articles to: RHBG Blocking Peptide
- In seahorses (family Syngnathidae), the male brood pouch provides a protected environment for developing embryos. During pregnancy, embryos develop within an enclosed brood pouch, requiring a physiological mechanism to eliminate the nitrogenous waste excreted by the embryos. This study investigated the expression and localization of rhesus (Rh) glycoproteins, expected to function as ammonia transporters, in the brood pouch of the pot-bellied seahorse Hippocampus abdominalis. The expression of the RhAG, RhBG, and RhCG2 genes in the pouch was confirmed by reverse transcription-polymerase chain reaction (RT-PCR). In situ hybridization and immunohistochemistry revealed that RhBG and RhCG2 are localized in the inner epithelium of the pouch, while RhAG is present in erythrocytes and the endothelium of the blood vessels. Based on these findings, we propose the following waste removal pathway. Ammonia, presumably released from the embryo, would be transported from the lumen of the pouch through apical RhCG2 and basolateral RhBG of inner epithelial cells into the connective tissue beneath the inner epithelium. In the connective tissue, ammonia passes through RhAG-expressing endothelial cells into the vascular lumen and is likely taken up by RhAG-expressing erythrocytes, which then travel to the gills via the bloodstream. Then, ammonia is released from the RhAG-expressing erythrocytes through RhAG-expressing pillar cells, basolateral RhBG- and apical RhCG2-expressingpavement cells, finally into the surrounding seawater. This study provides a first molecular and cellular basis for a proposed ammonia removal mechanism within the seahorse brood pouch, highlighting physiological adaptations associated with male pregnancy in syngnathid fish. - Source: PubMed
Publication date: 2026/09/07
Yamazaki HirokiHiroi JunyaYasumasu ShigekiKawaguchi Mari - Rhesus (Rh) family B glycoprotein (RHBG) is a conserved ammonium transporter of the Rhesus family with established roles in systemic acid-base regulation. Although Rh family members are expressed in the male reproductive tract, the physiological role of RHBG in spermatogenesis and sperm function remains unclear. To investigate its role in male reproduction, Rhbg-/- mice were generated using clustered regularly interspaced short palindromic repeats/CRISPR-associated protein 9 (CRISPR/Cas9)-mediated gene editing, and male fertility and reproductive phenotypes were assessed by breeding assays, histological analyses of the testes and epididymides, sperm morphology evaluation, computer-assisted sperm analysis during capacitation, and transmission electron microscopy of flagellar ultrastructure. Rhbg-/- male mice showed largely preserved fertility and produced offspring numbers comparable to those of wild-type controls, although a modest reduction in litter size was observed. Consistently, testicular architecture, spermatogenesis, and epididymal morphology were normal, and transmission electron microscopy confirmed intact flagellar ultrastructure. Computer-assisted sperm analysis further showed normal progressive motility under both basal and capacitating conditions. However, under hyperactivation-associated conditions, Rhbg-/- sperm exhibited a mild reduction in total motility, accompanied by subtle decreases in straight-line velocity and straightness. In addition, a slight increase in tail-coiling abnormalities was observed, whereas overall sperm morphology remained largely normal. Together, these findings indicate that Rhbg is not essential for spermatogenesis or male fertility in mice, but its absence causes minor, context-dependent alterations in sperm trajectory efficiency during capacitation without affecting core motility or ultrastructural integrity. Thus, RHBG may contribute to the fine regulation of sperm motility behavior rather than acting as a major determinant of reproductive capacity. - Source: PubMed
Publication date: 2026/09/04
Tan Guang-QingChen Lu-JieYang RuiDong YueZhang Jin-TaoLiu Ming-XiYang Xiao-Yu - Breast cancer remains a leading cause of cancer-related mortality worldwide, highlighting the need for novel therapeutic strategies that selectively target tumor cells while minimizing systemic toxicity. Dietary ammonium hydroxide enhancement (AHE) has previously been shown to modulate metabolic pathways in animal studies. However, its potential as a localized anticancer therapy has not been investigated. In the present study, we evaluated the antitumor efficacy and systemic safety of NHOH using complementary in vitro and orthotopic breast cancer xenograft models. MDA-MB-231 breast cancer cells and non-tumorigenic MCF10A mammary epithelial cells were treated with increasing concentrations of NHOH (2.5-225 µM) to assess dose-dependent effects on cell proliferation, viability, and apoptosis. Following this, MDA-MB-231 cells were orthotopically xenografted into female athymic nude mice and treated by intratumoral injection with NHOH using a stepwise dose-escalation regimen (0.01%, 0.1%, and 0.5%; total volume of 20 μL per tumor divided between two injection sites) or phosphate-buffered saline (PBS). Differences between treatment groups of mammary tumors and kidney tissues were analyzed molecularly and histologically. NHOH significantly suppressed MDA-MB-231 cell growth and metabolic activity, with minimal effects on MCF10A cells, and induced apoptosis in MDA-MB-231 cells without detectable apoptotic induction in MCF10A cells. In vivo, although tumor volume only showed a non-significant downward trend, histological and molecular analyses demonstrated substantial alterations in tumor biology. NHOH treatment induced molecular changes consistent with an antitumor response, including increased Caspase-3 and p53 expression, reduced BCL2 and Ki-67 expression, and attenuation of TNFα, IL-6, and TLR4 inflammatory signaling. Furthermore, the tumor architecture in T-NH tumors displayed increased pale eosinophilic regions and reduced cellular density, suggestive of treatment-associated tumor tissue disruption. Histological analysis of kidney tissue showed no evidence of overt renal toxicity. Indeed, localized NHOH administration was associated with reduced renal inflammatory and apoptotic signaling, preserved renal morphology, and increased expression of the ammonia transporters RHBG and RHCG. Cross-sectional morphometric measurements showed decreased area for the distal convoluted tubules in NHOH-treated samples. Although this initial preclinical study was limited by a relatively small sample size, further studies are warranted to validate these findings and define the molecular mechanisms underlying NHOH-mediated antitumor activity. Collectively, these findings suggest that intratumoral NHOH modulates tumor metabolic, inflammatory, and apoptotic pathways associated with a less aggressive tumor phenotype while showing no overt molecular or histological evidence of renal injury, supporting further investigation as a localized metabolic intervention targeting molecular and histological drivers of breast cancer progression. - Source: PubMed
Publication date: 2026/08/07
Deshmukh HemalataSchacherer CamilleYeom KyunghoonRivera AlainaOlayiwola YusuffGollahon Lauren - Sex-dependent differences are evident in most organs and contribute to variability in physiological function and disease susceptibility, which can consequently affect therapeutic responses. The kidney is no exception to this finding and recent data suggest that sexual dimorphism exists in the regulation of acid-base homeostasis. - Source: PubMed
Publication date: 2026/07/01
Halter Rebecca ZoeNogueira Coelho JenniferDominguez Rieg Jessica ARieg Timo - : Genetic generalized epilepsies (GGE) often remit in childhood, yet a subset of adults remain pharmacoresistant with substantial morbidity. The genetic basis of adult pharmacoresistant GGE is poorly defined. This descriptive study used whole-genome sequencing (WGS) to identify recurrent coding variants and pathways associated with pharmacoresistant adult GGE. : WGS was performed in ten racially diverse adults (mean age 37.2 years; range 20-52) with electroencephalographically confirmed, pharmacoresistant GGE (mean onset 13.7 years). Analysis prioritized variants present in at least 80% of participants and which were either (i) missense variants predicted deleterious with ANNOVAR or (ii) loss-of-function variants predicted high-impact from snpEff. Pathway enrichment and overlap with a commercial clinical epilepsy gene panel were assessed. : Filtering identified 133 unique, deleterious coding variants across 69 genes shared by at least eight participants. Four genes (APOL4, KMT2C, SON, VDR) overlapped a clinical epilepsy panel, supporting the capacity of WGS to recover clinically relevant loci. Prioritized loci implicated gastrointestinal and metabolic regulators (e.g., MUC6, PNLIPRP2), chemosensory receptors (OR10D3, OR8U1, TAS2R19), neuroimmune mediators (LILRA2, SIGLEC12, OAS2), and ion transporters (KCNJ12, P2RX5, RHBG), consistent with multifactorial mechanisms of pharmacoresistance. : This exploratory WGS study focused exclusively on adults with pharmacoresistant GGE, revealing shared high-impact variants and convergent pathways spanning absorption/metabolism, vitamin D signaling, immunity, and ion transport. Findings broaden the genetic landscape of pharmacoresistant GGE while motivating validation in larger, multiethnic cohorts. - Source: PubMed
Publication date: 2026/05/14
Kidder Benjamin LXu JianGeng RuiDlugas HunterVavilikolanu AnushaChen WeiWasade Vibhangini S