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this study shows that TGF-beta suppresses RasGRP1 expression and supports regulatory T cell resistance against p53-induced CD28-dependent T-cell apoptosis
guanine nucleotide exchange factor RasGRP1 inhibited Rhes-mediated control of striatal motor activity in mice. RasGRP1 stabilized Rhes, increasing its synaptic accumulation in the striatum.
signaling underpins thymic selection processes induced by both weak and strong TCR signals and is differentially required for fate decisions derived from a strong TCR stimulus
RasGRP1/3-deficient progenitors show impaired migration toward the CCR9 ligand, CCL25, suggesting that RasGRP1 and RasGRP3 may regulate progenitor entry into the thymus through a CCR9-dependent mechanism.
RasGRP1 is indispensable for development of B1a cells with autoantigen receptors, revealing a connection between a signaling molecule and development of a specific repertoire within the B1a cell population
Genetic Rasgrp1 depletion from mice with either an activating mutation in KRas or with aberrant Wnt signalling due to a mutation in Apc resulted in both cases in exacerbated Ras-ERK signalling and cell proliferation.
CD44 expression, CD4(+) T cell subset ratios and serum autoantibodies all returned to normal in Rasgrp1(Anaef)Mtor(chino) double-mutant mice
RasGRP1 upregulates signaling from Ras and contributes to epidermal tumorigenesis by increasing the total dosage of active Ras.
autoreactive B cells lacking Rasgrp1 break central and peripheral tolerance through both T cell-independent and -dependent mechanisms.
Dysregulated RasGRP1 responds to cytokine receptor input in T cell leukemogenesis.
RasGRP1, but not RasGRP3, is required for thymocyte positive selection and invariant natural killer T cell selection.
Genetic analysis shows that disease progression and ERK signaling are dependent on RAS guanine exchange factor responsible for ERK activation and lymphoproliferative phenotype in LAT-Y136F mutant mice.
While the DAG-binding C1 domain of RasGRP1 has long been recognized as an important factor mediating Erk activation, we have revealed the physiological relevance of the tail domain in RasGRP1 function and control of Erk signaling
assessed the independent and combined roles for the RasGEFs Sos1, Sos2, and RasGRP1 during thymocyte development
RasGRP1 plays differential roles for gammadelta and alphabeta T cell development but is critical for gammadeltaT cell proliferation and production of IL-17.
RasGRP1 is important not only for early invariant natural killer (NK)T cell development but also for the generation and maintenance of CD4-positive NKT cells.
Gene silencing of Ras-GRP1 prevented the PTH-mediated suppression of NCC activity, the activation of the H-Ras isoform of Ras, and the activation of ERK1/2 MAPK
Data found that a basic/hydrophobic cluster of amino acids within the plasma membrane-targeting domain of RasGRP1 is instead responsible for plasma membrane targeting.
Phorbol ester-mediated sodium chloride cotransporter NCC endocytosis is dependent on ubiquitination via RasGRP1-mediated ERK1/2 activation.
RasGRP1 is essential for ras activation by the tumor promoter 12-O-tetradecanoylphorbol-13-acetate in epidermal keratinocytes.
RASGRP1 deficiency is associated with life-threatening immune dysregulation, severe autoimmune manifestations, and susceptibility to EBV-induced B cell malignancies. Early diagnosis is critical and hematopoietic stem cell transplantation might be considered as curative treatment.
this study shows that RASGRP1 mutation should be considered in patients with autoimmune lymphoproliferative syndrome-like disease
SRSF1 expression levels were significantly lower in T cells from systemic lupus erythematosus (SLE) patients compared to healthy subjects, and correlated inversely with disease activity and positively with levels of RasGRP1-WT and DNMT1. AS to RasGRP1-WT and decreased levels of RasGRP1 protein, whereas overexpression of SRSF1 in SLE T-cells caused recovery of RasGRP1, which in turn induced DNMT1/interleukin-2 expression.
RasGRP1 overexpression was an independent prognostic factor in hepatocellular carcinoma (HCC) patients. RasGRP1 is upregulated in HCC and promotes HCC cell proliferation. Thus, RasGRP1 may be a novel therapeutic target for HCC.
Histidine 212 is located at the fulcrum of these conformational changes, and structural features in its vicinity are consistent with its function as a pH-dependent switch.
The rs7170151 in RASGRP1 showed novel associations in IgA nephropathy.
The marked differences between RasGRP3 and RasGRP1 in membrane interaction necessarily will contribute to their different behavior in cells.
Cytokines IL-2/7/9 stimulation activates PI3K/Akt pathways downstream of Ras in RasGRP1 T-cell acute lymphoblastic leukemia (T-ALL).
results demonstrate the critical role of CalDAG-GEFI in rapid alphaIIbbeta3 activation of human platelets.
Low-level expression of CD-GEFI impairs platelet activation, leading to protection from thrombosis, but not to marked bleeding in mice.
This study shows that deficiency in RASGRP1 results in a previously unknown primary immunodeficiency disease, and that RASGRP1 plays role in immune cell signaling and function in T cells, B cells and NK cells. It also identifies a previously unknown role for RASGRP1 in the dynamic regulation of the cytoskeleton, and identify lenalidomide as a potpotential treatment option for this immunodeficiency.
This study aimed to replicate and verify the association of RASGRP1 tag single-nucleotide polymorphisms with T2D in a Chinese Han population.
present a crystal structure of a fragment of RasGRP1 in which the Ras-binding site is blocked by an interdomain linker and the membrane-interaction surface of RasGRP1 is hidden within a dimerization interface
A genome-wide association study identifies GRK5 and RASGRP1 as type 2 diabetes loci in Chinese Hans.
This is the first study aimed at evaluating CalDAG-GEFI gene sequences in people with mucocutaneous bleeding of unknown cause.
PAQR10 and PAQR11 are able to interact with RasGRP1, a guanine nucleotide exchange protein of Ras, and increase Golgi localization of RasGRP1. The C1 domain of RasGRP1 is both necessary and sufficient for the interaction of RasGRP1 with PAQR10/PAQR11.
cooperation between aberrant expression of RasGRP1, a strong activator of Ras, and secondary gain-of-function mutations of NOTCH1 have an important role in T-cell leukemogenesis
remission in systemic lupus erythematosus activity associated with decreased RasGRP-1 expression in lymphocytes
Basal LAT-diacylglycerol-RasGRP1 signals in T cells maintain TCRalpha gene expression.
SDF-1 treatment of T cells induced the formation of a novel molecular signaling complex containing RasGRP1, Galphai2, and ZAP-70.
This gene is a member of a family of genes characterized by the presence of a Ras superfamily guanine nucleotide exchange factor (GEF) domain. It functions as a diacylglycerol (DAG)-regulated nucleotide exchange factor specifically activating Ras through the exchange of bound GDP for GTP. It activates the Erk/MAP kinase cascade and regulates T-cells and B-cells development, homeostasis and differentiation. Alternatively spliced transcript variants encoding different isoforms have been identified. Altered expression of the different isoforms of this protein may be a cause of susceptibility to systemic lupus erythematosus (SLE).
RAS guanyl-releasing protein 1
, calcium and DAG-regulated guanine nucleotide exchange factor II
, RAS guanyl nucleotide-releasing protein 1
, guanine nucleotide exchange factor, calcium- and DAG-regulated, Rap1A
, ras activator RasGRP