about
Characterization of p87C3G, a novel, truncated C3G isoform that is overexpressed in chronic myeloid leukemia and interacts with Bcr-AblMet signaling in cardiomyocytes is required for normal cardiac function in adult miceC3G forms complexes with Bcr-Abl and p38α MAPK at the focal adhesions in chronic myeloid leukemia cells: implication in the regulation of leukemic cell adhesion.C3G-mediated suppression of oncogene-induced focus formation in fibroblasts involves inhibition of ERK activation, cyclin A expression and alterations of anchorage-independent growth.Risk factors for thrombotic microangiopathy in allogeneic hematopoietic stem cell recipients receiving GVHD prophylaxis with tacrolimus plus MTX or sirolimus.Incidence and risk factors for life-threatening bleeding after allogeneic stem cell transplant.The CRISPR/Cas9 system efficiently reverts the tumorigenic ability of BCR/ABL in vitro and in a xenograft model of chronic myeloid leukemia.Serum-dependent transcriptional networks identify distinct functional roles for H-Ras and N-Ras during initial stages of the cell cycleAnalysis of incidence, risk factors and clinical outcome of thromboembolic and bleeding events in 431 allogeneic hematopoietic stem cell transplantation recipientsNADPH oxidases as therapeutic targets in chronic myelogenous leukemia.C3G down-regulates p38 MAPK activity in response to stress by Rap-1 independent mechanisms: involvement in cell death.C3G silencing enhances STI-571-induced apoptosis in CML cells through p38 MAPK activation, but it antagonizes STI-571 inhibitory effect on survival.p38 MAPK down-regulates fibulin 3 expression through methylation of gene regulatory sequences: role in migration and invasion.C3G mediated suppression of malignant transformation involves activation of PP2A phosphatases at the subcortical actin cytoskeleton.C3G transgenic mouse models with specific expression in platelets reveal a new role for C3G in platelet clotting through its GEF activity.C3G promotes a selective release of angiogenic factors from activated mouse platelets to regulate angiogenesis and tumor metastasis.How Rap and its GEFs control liver physiology and cancer development. C3G alterations in human hepatocarcinomaC3G, through its GEF activity, induces megakaryocytic differentiation and proplatelet formationRisk of placenta-mediated pregnancy complications or pregnancy-related VTE in VTE-asymptomatic families of probands with VTE and heterozygosity for factor V Leiden or G20210 prothrombin mutationC3G contributes to platelet activation and aggregation by regulating major signaling pathways
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P50
description
researcher, ORCID id # 0000-0002-8747-6831
@en
wetenschapper
@nl
name
Carmen Guerrero
@ast
Carmen Guerrero
@en
Carmen Guerrero
@es
Carmen Guerrero
@nl
type
label
Carmen Guerrero
@ast
Carmen Guerrero
@en
Carmen Guerrero
@es
Carmen Guerrero
@nl
prefLabel
Carmen Guerrero
@ast
Carmen Guerrero
@en
Carmen Guerrero
@es
Carmen Guerrero
@nl
P106
P1153
7005721690
P31
P496
0000-0002-8747-6831