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Angiogenic factor with G patch and FHA domains 1

AGGF1, VG5Q, angiogenic factor with G-patch and FHA domains 1, angiogenic factor VG5Q
This gene encodes an angiogenic factor that promotes proliferation of endothelial cells. Mutations in this gene are associated with a susceptibility to Klippel-Trenaunay syndrome. Pseudogenes of this gene are found on chromosomes 3, 4, 10 and 16.[provided by RefSeq, Sep 2010] (from NCBI)
Top mentioned proteins: vascular endothelial growth factor, KDR, GATA-1, p53, HAD
Papers on AGGF1
Overexpression of AGGF1 is correlated with angiogenesis and poor prognosis of hepatocellular carcinoma.
Ji et al., Hefei, China. In Med Oncol, Apr 2015
Angiogenic factor with G-patch and FHA domains 1 (AGGF1) is a factor implicating in vascular differentiation and angiogenesis.
X-linked thrombocytopenia with thalassemia displays bone marrow reticulin fibrosis and enhanced angiogenesis: comparisons with primary myelofibrosis.
Palmblad et al., Örebro, Sweden. In Am J Hematol, Mar 2015
Further, as evaluated by immunohistochemistry, expressions of the growth factors VEGF, AGGF1, and CTGF were low in XLTT megakaryocytes and microvessels but high in PMF.
β-Catenin-dependent transcription is central to Bmp-mediated formation of venous vessels.
Mochizuki et al., Suita, Japan. In Development, Mar 2015
During caudal vein (CV) formation, Bmp induces the expression of aggf1, a putative causative gene for Klippel-Trenaunay syndrome, which is characterized by venous malformation and hypertrophy of bones and soft tissues.
Foot ulcers in klippel-trenaunay syndrome: two case reports and one metatypical Basal cell carcinoma.
Wollina et al., Dresden, Germany. In J Biol Regul Homeost Agents, 2015
Klippel-Trenaunay syndrome (KTS) is a congenital malformation with vascular anomalies of capillaries, veins and lymphatics and hypertrophy of bones and soft tissues, associated with microdeletion of 2q37.3 and upregulation of angiogenic factor AGGF1.
AGGF1 protects from myocardial ischemia/reperfusion injury by regulating myocardial apoptosis and angiogenesis.
Li et al., Beijing, China. In Apoptosis, 2014
Angiogenic factor with G patch and FHA domains 1 (AGGF1) is a newly identified proangiogenic protein, which plays an important role in vascular disease and angiogenesis.
Role of microRNA-27a in down-regulation of angiogenic factor AGGF1 under hypoxia associated with high-grade bladder urothelial carcinoma.
Wang et al., Wuhan, China. In Biochim Biophys Acta, 2014
Surprisingly, here we report significant association between down-regulation of a new angiogenic factor AGGF1 and high-grade urothelial carcinoma.
Aggf1 acts at the top of the genetic regulatory hierarchy in specification of hemangioblasts in zebrafish.
Wang et al., Wuhan, China. In Blood, 2014
Here we show that aggf1 acts at the top of the genetic regulatory hierarchy in the specification of hemangioblasts in zebrafish.
Genomic scan reveals loci under altitude adaptation in Tibetan and Dahe pigs.
Ma et al., Beijing, China. In Plos One, 2013
Totally, we identified 12 specific selective genes (CCBE1, F2RL1, AGGF1, ZFPM2, IL2, FGF5, PLA2G4A, ADAMTS9, NRBF2, JMJD1C, VEGFC and ADAM19) for TBP and six (OGG1, FOXM, FLT3, RTEL1, CRELD1 and RHOG) for DHP.
AGGF1 is a novel anti-inflammatory factor associated with TNF-α-induced endothelial activation.
Tian et al., Beijing, China. In Cell Signal, 2013
AGGF1, a new member of angiogenic factors with a FHA and a G-patch domain, has been shown critical for the regulation of vascular differentiation and angiogenesis.
Functional characterization of Klippel-Trenaunay syndrome gene AGGF1 identifies a novel angiogenic signaling pathway for specification of vein differentiation and angiogenesis during embryogenesis.
Wang et al., Wuhan, China. In Hum Mol Genet, 2013
We have previously reported that upregulation of angiogenic factor AGGF1 is associated with KTS, but the molecular mechanism is not clear.
Angiogenic factor AGGF1 promotes therapeutic angiogenesis in a mouse limb ischemia model.
Wang et al., Wuhan, China. In Plos One, 2011
In this study, we assessed the potential of a new angiogenic factor AGGF1 for therapeutic angiogenesis in a critical limb ischemia model in mice for PAD.
Sphingolipid modulation of angiogenic factor expression in neuroblastoma.
Ferrer et al., Farmington, United States. In Cancer Prev Res (phila), 2011
Sphingolipid modulation of angiogenic factor expression in neuroblastoma
Effects of hyperprolactinemia treatment with the dopamine agonist quinagolide on endometriotic lesions in patients with endometriosis-associated hyperprolactinemia.
Pellicer et al., Valencia, Spain. In Fertil Steril, 2011
Histologic analysis showed tissue degeneration, which was supported by down-regulation of VEGF/VEGFR2, three proangiogenic cytokines (CCL2, RUNX1, and AGGF1) and plasminogen activator inhibitor (PAI) 1, a potent inhibitor of fibrinolysis in the L2 lesions.
Novel roles of GATA1 in regulation of angiogenic factor AGGF1 and endothelial cell function.
Wang et al., Cleveland, United States. In J Biol Chem, 2009
Knockdown of GATA1 expression by siRNA reduced expression of AGGF1, and resulted in endothelial cell apoptosis and inhibition of vessel formation.
Identification of association of common AGGF1 variants with susceptibility for Klippel-Trenaunay syndrome using the structure association program.
Wang et al., Cleveland, United States. In Ann Hum Genet, 2008
identified two tagSNPs, rs13155212 and rs7704267 that capture information for all common variants in AGGF1 as a candidate susceptibility gene for Klippel-Trenaunay syndrome
Klippel-Trenaunay syndrome: a multisystem disorder possibly resulting from a pathogenic gene for vascular and tissue overgrowth.
Janniger et al., Newark, United States. In Int J Dermatol, 2006
This review describes the somatic mutation for angiogenic factor VG5Q, which may be the cause of the multisystem disorder Klippel-Trenaunay syndrome.
Is the E133K allele of VG5Q associated with Klippel-Trenaunay and other overgrowth syndromes?
Harper et al., In J Med Genet, 2006
VG5Q, E133K is a mutation that causes Klippel-Trenaunay and other overgrowth syndromes.
Biomedicine and diseases: the Klippel-Trenaunay syndrome, vascular anomalies and vascular morphogenesis.
Wang et al., Cleveland, United States. In Cell Mol Life Sci, 2005
A susceptibility gene, VG5Q (formally named AGGF1), was cloned for Klippel-Trenaunay syndrome (KTS).
Update on the molecular genetics of vascular anomalies.
Wang, Cleveland, United States. In Lymphat Res Biol, 2004
These genes include AGGF1 for Klippel-Trenaunay syndrome, RASA1 for capillary malformations, KRIT1, MGC4607, PDCD10 for cerebral cavernous malformations, glomulin for glomuvenous malformations, TIE2 for multiple cutaneous and mucosal venous malformations, VEGFR-3, FOXC2, NEMO, SOX18 for lymphedema or related syndromes, ENG, ACVRLK1, MADH4 for HHT or related syndromes, NDP for Coats' disease, Notch3 for CADASIL, and PTEN for Proteus Syndrome.
Identification of an angiogenic factor that when mutated causes susceptibility to Klippel-Trenaunay syndrome.
Wang et al., Cleveland, United States. In Nature, 2004
results define VG5Q as an angiogenic factor, establish VG5Q as a susceptibility gene for Klippel-Trenaunay syndrome, and show that increased angiogenesis is a molecular pathogenic mechanism of KTS
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