RASGRP2 antibody
- Known as:
- RASGRP2 (anti-)
- Catalog number:
- orb30159
- Product Quantity:
- 20 ug(Trial size)
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- RASGRP2 antibody
Related genes to: RASGRP2 antibody
- Gene:
- RASGRP2 NIH gene
- Name:
- RAS guanyl releasing protein 2
- Previous symbol:
- -
- Synonyms:
- CALDAG-GEFI
- Chromosome:
- 11q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-07-21
- Date modifiied:
- 2019-04-23
Related products to: RASGRP2 antibody
Related articles to: RASGRP2 antibody
- Deep infiltrating endometriosis (DIE) is a highly fibrotic and deeply invasive subtype of endometriosis that causes severe pelvic pain, infertility and marked impairment of quality of life. Metabolic, microbial and immune disturbances have been reported in women with endometriosis, but whether these systemic perturbations causally contribute to DIE and which lesion-level molecular mediators connect them to pelvic pathology remains unknown. - Source: PubMed
Publication date: 2026/05/21
Shi ShanpingSong WeiWu ZhipingCheng YufengLiu HuaTian FujuLi Xiaocui - Amyotrophic lateral sclerosis (ALS) lacks reliable, disease-specific, and minimally invasive biomarkers, representing a major barrier to early diagnosis and patient stratification. The primary aim of this translational pilot study was to identify a disease-specific, TDP-43-related, gene-microRNA (miRNA) signature in peripheral blood mononuclear cells (PBMCs) of ALS patients with potential diagnostic value. To this end, we first identified differentially expressed disease-specific genes (dsDEGs) using a TDP-43-based rat model of ALS, generated by stereotaxic infusion of full-length (FL) TAR DNA-binding protein 43 (TDP-43) into the motor cortex. Transcriptomic profiling of the motor cortex revealed candidate dsDEGs, which were subsequently validated by RT-qPCR in motor cortex, spinal cord, and PBMCs from the same animals. To assess translational relevance, expression levels of these dsDEGs were analyzed in PBMCs from early- to mid-stage ALS patients and matched healthy controls, while disease specificity was evaluated using Parkinson's disease (PD) samples. In parallel, conserved miRNAs predicted to target the identified dsDEGs were examined in both rat and human PBMCs. Five dsDEGs, Mctp1, Penk, Mt2A, Drd1, and Rasgrp2, were consistently dysregulated across central and peripheral tissues in the TDP-43 rat model. RT-qPCR analysis of human PBMCs confirmed significant and selective dysregulation of these genes in ALS, but not in PD, supporting disease specificity. Moreover, exposure of human neuroblastoma cells and healthy PBMCs to TDP-43 recapitulated the ALS-like expression changes. Computational and experimental analyses identified seven conserved miRNAs targeting these dsDEGs, of which four were significantly downregulated in ALS PBMCs, supporting a coordinated regulatory network. Receiver operating characteristic (ROC) analyses demonstrated strong discriminative performance for both the gene signature (AUC 0.87-1.00) and the associated miRNAs (AUC 0.95-1.00). Together, these findings define a novel PBMC-based gene-miRNA signature that mirrors central ALS pathology and shows high diagnostic accuracy and disease specificity, highlighting its potential as a minimally invasive biomarker for ALS. - Source: PubMed
Publication date: 2026/06/06
Manchinu Maria FrancescaCongiu MichelaMassidda MatteoBorghero GiuseppeMarongiu JacopoMarzi IsabellaMaschio AndreaRallo VincenzoSerra MarcelloPorcedda ClaraEtzi MichelaPalmas Maria FrancescaAngius AndreaSogos ValeriaPateri Maria IdaSteri MaristellaCoroneo ValentinaDe Simone AlfonsoCossu GiovanniChiti FabrizioCarta Anna Rosa - Due to the substantial secretory burden, bovine mammary epithelial cells (BMECs) are highly susceptible to endoplasmic reticulum (ER) stress caused by the accumulation of misfolded proteins when protein-folding capacity is overwhelmed. However, how ATF3 regulates ER stress-induced impairment of milk synthesis and apoptosis in BMECs, particularly through its direct transcriptional targets, remains poorly understood. In this study, we investigated the protective role of activating transcription factor 3 (ATF3) against ER stress-induced impairment of milk synthesis in BMECs. Using a tunicamycin-induced ER stress model, we overexpressed in BMECs and performed integrated RNA-seq and ChIP-seq analyses to elucidate the underlying molecular mechanisms. Our results indicated that ER stress disrupted milk protein and fat synthesis in BMECs by suppressing the expression of CSN2, FASN, FABP3 and promoting apoptosis via upregulation of BAX and CASP3. overexpression effectively attenuated these effects, reducing apoptosis and restoring the expression of milk fat-related genes. Transcriptomics demonstrated that ATF3 activated MAPK and PI3K-Akt signaling and lipid metabolism pathways, significantly upregulating key genes involved in fatty acid uptake, transport, and metabolism (, , , ). Integrated RNA-seq and ChIP-seq analyses identified 81 overlapping genes, with , , , and confirmed as direct transcriptional targets of ATF3, mediating its regulation of the MAPK pathway. Collectively, these findings elucidate the protective role of ATF3 against ER stress-induced lactation disruption and offer potential molecular targets for enhancing lactation resilience in dairy cattle under stress. - Source: PubMed
Publication date: 2026/05/10
Zhang ChenDai WentingLiu YueXu HongweiLiu Hongyun - This study retrospectively analyzed a 4-year-and-8-month-old boy with RASGRP2-associated inherited platelet function disorders (IPFD) who was successfully treated with allogeneic hematopoietic stem cell transplantation, along with a review of the relevant literature. The patient presented with a 3-year history of recurrent epistaxis, and following comprehensive evaluation, he was diagnosed as having RASGRP2-related IPFD. Because of life-threatening bleeding risk and poor response to conventional treatment, an HLA-matched sibling without the pathogenic variant was selected as the donor, and a myeloablative conditioning regimen was administered. Platelet engraftment was achieved on Day 13 posttransplantation, and neutrophil and erythrocyte engraftment occurred on Day 18. Donor chimerism reached 99.7% on Day 22. Epistaxis during conditioning was controlled with nasal packing and platelet transfusion, and no bleeding recurred after platelet engraftment. At the 4-month follow-up, no graft-versus-host disease or severe infection was detected, and complete donor chimerism was confirmed. - Source: PubMed
Wang C LMeng L HXia WLong S QFang C YLiang X L - Identifying autoantigens in multiple sclerosis (MS) has been challenging. If successful, this could facilitate development of autoantigen-specific tolerogenic therapies, by exposing antigen presenting cells (APC) to tolerogenic stimuli with autoantigens specific to the human leukocyte antigen (HLA) haplotype of patients. RAS guanyl releasing protein 2 (RASGRP2), which is expressed by lymphocytes and striatal neurons, is a putative autoantigen in HLA-DRB1*15:01 (DR15)-positive individuals. We aimed to identify antigenic RASGRP2 epitope(s) that could be used to develop tolerogenic therapies. RASGRP2-derived peptides of varying DR15 binding affinities were exposed to peripheral blood mononuclear cells (PBMCs). Immunoeptidomic techniques demonstrated strong and moderate binding affinity RASGRP2 peptides could be presented by HLA-DR on PBMCs from DR15-homozygous or DR15-negative patients. Moderate affinity peptides produced the greatest increase in CD80 expression and pro-inflammatory cytokine (IFN-γ, IL-17, IL-22) secretion by PBMCs, particularly in DR15-positive patients. One RASGRP2 peptide eliciting the highest pro-inflammatory responses was used to generate HLA-DR15 tetramers. CD4+ T-cells specific for this peptide were four-fold higher in frequency in DR15-positive patients versus controls, more pro-inflammatory in phenotype and demonstrated increased peptide-stimulated proliferation. In conclusion, we identified a novel immunogenic RASGRP2 peptide with relative selectivity for HLA-DR15-positive people with MS, which could form the basis for autoantigen-specific tolerogenic therapy. - Source: PubMed
Publication date: 2026/05/15
Li VivienPandey KirtiBinder Michele DReid Hugh HLim Jia JiaLoh Tiing JenTran Mai TRossjohn JamiePurcell Anthony WKilpatrick Trevor J