RASGRP2
- Known as:
- RASGRP2
- Catalog number:
- ARP58820_P050
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- RASGRP2
Related genes to: RASGRP2
- 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
Related articles to: RASGRP2
- 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 - Hemostasis and thrombosis are strongly dependent on the unique ability of platelets to rapidly activate integrin receptors and to firmly adhere to sites of injury under shear stress conditions. Central to integrin activation is the small GTPase RAP1, which itself is activated by guanine nucleotide exchange factors (GEFs). CalDAG-GEFI (RASGRP2) is the highest expressed and functionally dominant platelet RAP-GEF. However, a genome-wide association study also suggested a significant role for RAPGEF2 (PDZ-GEFI), a low expressed RAP-GEF, in human platelet aggregation. Here, we used mice deficient in RAPGEF2 (megakaryocyte-specific, Rapgef2mKO), CalDAG-GEFI (Caldaggef1-/-), or both RAPGEF2 and CalDAG-GEFI (DKO) to characterize the contribution of RAPGEF2 signaling to platelet function, hemostasis and thrombosis. RAPGEF2 protein was detected in murine and human platelets. Compared to control or Caldaggef1-/- platelets, both RAP1 activation and integrin aIIbb3-mediated aggregation were significantly diminished in DKO platelets. When compared to controls, Rapgef2mKO platelets exhibited reduced integrin activation, a more reversible aggregation response, and impaired adhesion under conditions of shear stress ex vivo and in vivo. Mechanistic studies strongly suggest that RAPGEF2 operates downstream of receptors coupled to the heterotrimeric G protein, G13 (GNA13), such as aIIbb3 and the thromboxane receptor. Together, our studies provide genetic evidence that RAPGEF2 in platelets operates downstream of G13 as an important regulator of RAP1 signaling and integrin activation, especially under conditions of elevated shear stress. These findings markedly improve our understanding of G protein signaling and integrin function in platelets, with potential implications for the development of improved platelet-targeted therapies for cardiovascular disease. - Source: PubMed
Publication date: 2026/04/08
Paul David SRocco David JClark Emily GSchug Wyatt JMartyanov Alexey AVander Ploeg Matthew RJones Summer RLee Robert HMwiza Jean Marie NBallard-Kordeliski AbigailDeger NazliKawano TomohiroMackman NigelBergmeier Wolfgang - Immediate-early gene (IEG) induction guides elucidation of signaling pathways mediating neuronal plasticity underlying compulsive use of psychostimulants. IEG induction after psychostimulant administration has been attributed to both PKA- and RapGEF2-dependent signaling pathways initiated by D1 receptor stimulation by dopamine. However, it is not clear how each pathway contributes individually to IEG induction, dopaminoceptive neuronal activity, and neuronal plasticity. We used Cre-LoxP technology and a novel Cre-amplifier transgene to delete RapGEF2 only in D1-MSNs, and investigate its role in cocaine-induced IEG and behavioral responses. D1-MSN-specific RapGEF2 deletion blocked cocaine-induced ERK phosphorylation and Egr-1 induction, without affecting cocaine self-administration or c-Fos induction by cocaine. Deletion of Rap1 in D1-MSNs blocked cocaine-induced p-ERK and Egr-1 expression, but not the induction of c-Fos. Like RapGEF2 deletion, Rap1 deletion from D1-MSNs had no effect on final maintenance of stable cocaine self-administration, although the rate of acquisition was significantly impaired. These results suggest that D1-dependent activation of Egr1 is not ultimately required for cocaine self-administration, although it may affect the behavioral dynamics of this process. Suppressing cAMP elevation in D1-MSNs by D1-specific expression of PDE4D3-cat greatly reduced induction of both Egr-1 and c-Fos in NAc after cocaine administration, demonstrating that induction of both IEGs requires cAMP elevation in D1-MSNs. Specific inhibition of PKA activity via PKI-alpha expression in D1-MSNs also blocked both c-Fos and Egr-1 induction. Thus, acute or chronic cocaine administration activates at least two separate cAMP effectors in D1-MSNs. PKA activation leads to c-Fos induction, likely through CREB, and to Egr1 activation via Rap1, likely through a previously reported dependence on RasGRP2. RapGEF2 activation leads exclusively to Egr1 induction. The finding that PKA activates the ERK-Egr-1 signaling pathway by convergence on Rap1, and concomitantly activates c-Fos independently of Rap1, may underlie selective effects of RapGEF2 and PKA inhibition on psychostimulant-dependent behaviors in mice. - Source: PubMed
Zhang Hai-YingSalman TabindaBi Guo-HuaJiang Sunny ZGerfen Charles RLutas AndrewXu WenqinXi Zheng-XiongEiden Lee E - Ovarian cancer is a rare cancer, it has the worst prognosis and the highest mortality rate, especially in high-grade serous ovarian cancer (HGSOC). High-throughput data generation is developed and provides an opportunity to investigate molecular pathways involved in cancer progression. The purpose of this study is to explore the role of main genes linked to the immune system and immune microenvironment in HGSOC using bioinformatics approaches to introduce promising biomarkers. - Source: PubMed
Publication date: 2025/11/28
Fatehi RaziehTabatabaiefar MohammadAminBehnamfar FaribaKhanahmad Hossein