Human R-Spondin 1 / RSPO1 Protein
- Known as:
- Human R-Spondin 1 / RSPO1 Protein
- Catalog number:
- RS1-H4221
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- acrobyosystems
- Gene target:
- Human R-Spondin 1 / RSPO1 Protein
Related genes to: Human R-Spondin 1 / RSPO1 Protein
- Gene:
- RSPO1 NIH gene
- Name:
- R-spondin 1
- Previous symbol:
- -
- Synonyms:
- FLJ40906, RSPONDIN
- Chromosome:
- 1p34.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-08-08
- Date modifiied:
- 2016-10-05
Related products to: Human R-Spondin 1 / RSPO1 Protein
Related articles to: Human R-Spondin 1 / RSPO1 Protein
- Endometrial injury (EI) is a primary cause of refractory infertility characterized by defective glandular regeneration and impaired receptivity, for which effective regenerative therapies remain limited. Here, we identify the depletion of stromal-derived RSPO1 as a conserved molecular defect driving the loss of glandular stemness in both murine models and patient samples. We further demonstrate that this regeneration failure is rooted in the disruption of the spatial organization within the peri-glandular niche. Mechanistically, injured glandular epithelia act as spatial regulators by activating a paracrine IL10-IL10R-CD26 signaling cascade that enzymatically shapes a localized CXCL12 gradient. This chemokine-guided mechanism governs the selective recruitment of CXCR4⁺ mesenchymal stromal cells (MSCs) to peri-glandular domains. Crucially, we reveal that MSC-mediated repair operates via a spatially restricted mechanism of action, where therapeutic efficacy hinges on precise niche targeting. Upon niche localization, MSC-delivered RSPO1 reconstitutes WNT-driven glandular regeneration and implantation competence. Leveraging this endogenous spatial guidance, we engineered CXCR4/RSPO1 dual-enhanced MSCs to overcome delivery constraints, significantly improving homing efficiency and functional recovery in refractory EI models. Validation in patient-derived biopsies and organoids confirms the translational relevance of the IL10-CXCL12-RSPO1 regenerative axis. Collectively, these findings establish spatially targeted cell delivery as a precision pharmacotherapy, providing a mechanistic foundation for treating refractory infertility. - Source: PubMed
Publication date: 2026/05/18
Liu JialiDang YueZhou CongtingLi ChuyuWei MengruLi ShiqiCui JiawenZhou QingqingYu YingWang FeiyiShang XinLi YantongWang JingZhou FangWang Guangji - This study aimed to identify genomic regions and candidate genes associated with body composition, and meat quality traits in Iberian pigs fattened in Montanera. A genome-wide association study (GWAS) was conducted on 528 pigs for 29 phenotypic traits using genomic data from the GGP Porcine HD Array. After quality control, 526 animals and 35,894 SNPs were retained for the association analysis. Despite the limitations of the genotyping chip used, which lacked coverage for Iberian-specific variants, the GWAS performed with GCTA software identified 165 SNPs significantly associated with 11 traits. Among these, 145 SNPs were clustered into 25 quantitative trait loci (QTL) regions. Five QTLs were identified for ham yield, containing genes such as KCNIP4, ZNF438, and PID1. Eight QTLs were associated with loin yield, with genes like PREX2, RSPO1, and PDE4B. One QTL was associated with shear force, and 16 QTLs were related to fatty acid composition. Genes linked to these traits included ELOVL6, associated with myristic and palmitic acids, and ADCY9 and ROBO1, associated with linoleic acid. Overall, these results provide novel genomic insights and markers that could enhance selection strategies in Iberian pig breeding programs, while highlighting the need for improved genomic tools tailored to local breeds. - Source: PubMed
Publication date: 2026/05/16
Palma-Granados PatriciaGarcía-Casco Juan MRamón ManuelDelgado-Gutiérrez Miguel ASánchez-Esquiliche FernandoMárquez AlbertoMuñoz María - Endometriosis is a highly prevalent, hormone-driven chronic disease characterized by the growth of endometrial tissue outside the uterine cavity. Despite its impact, the mechanisms underlying the disease’s pathogenesis remain poorly understood. We hypothesized that not only the ectopic endometrium of women with endometriosis differs from that of women without the disease, but also the eutopic endometrium. Accordingly, this study aimed to identify potential differences in basal expression of hormone receptors, their responses to hormonal treatment, as well as general morphology and growth factor dependencies among organoids derived from the endometrium of women without endometriosis and from the eutopic and ectopic endometrial tissues of patients with endometriosis. - Source: PubMed
Publication date: 2026/04/23
Cioraityte JusteSchröder LennardBeimenbetova ZeineshRückl Anna TBeyer SusanneBecker JohannaKolben ThomasMahner SvenKessler MirjanaKeckstein Simon - There is a dearth of knowledge on the genetic background of Indian 46,XX DSD patients with Mullerian agenesis (MA) and/or gonadal dysgenesis (GD). Being one of the key controlling genes in female sex determination/differentiation, there is a paucity of study regarding the association of RSPO1 variations with MA/GD. Hence in this study, we screened proximal as well as exonic regions of the RSPO1 gene in 25 Indian 46,XX DSD patients with MA and/or GD. - Source: PubMed
T S RagithaK S SunishDaniel SaleyF SarithaGilvaz SareenaK V DileepFrancis JijoPulikkottil Raphael VargheseRaveendran Suresh Kumar - Direct somatic cell-to-neuronal fate reprogramming (induced neurons, iNs) is valuable for translational and basic research. N-Methyladenosine (mA), the most prevalent mRNA epitranscriptomic modification, is critical for neural biology, but its role in iN reprogramming remains elusive. Using our induced retinal ganglion cell-like neuron (iRGC) system, we found dynamic mA epitranscriptomic adjustments during iRGC reprogramming. Mettl3, the core component of the mA methyltransferase complex, promoted iRGC fate reprogramming and axon development. Integrated RNA-seq/MeRIP-seq analyses and gene function interrogations identified three mA-modified genes (Prokr1, Rspo1, and Fmo2) as key mediators of Mettl3 effects. Collectively, our study elucidated the essential roles and molecular mechanisms of the mA epitranscriptomic modification in neuronal fate reprogramming and axon development. These findings could aid future investigations designed to improve neuronal fate and axon regeneration outcomes for therapeutic purposes to treat neurodegenerative diseases. - Source: PubMed
Publication date: 2026/03/05
Zhang KeLiang HuilinChen Shuyi