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Von Hippel-Lindau syndrome (VHL) is a dominantly inherited familial cancer syndrome predisposing to a variety of malignant and benign tumors. Additionally we are shipping VHL Antibodies (118) and VHL Proteins (7) and many more products for this protein.
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Loss of Vhl in mesenchymal progenitors of the limb bud caused severe fibrosis of the synovial joints and formation of aggressive masses with histologic features of mesenchymal tumors.
These data suggested that intestinal epithelial cells were injured after IM treatment through the pVHL overexpression-induced degradation of collagen I or HIF-1alpha (show HIF1A ELISA Kits).
Vhl and Kif3a (show KIF3A ELISA Kits) deletion accelerates renal cyst formation
maintains the stability and suppressive function of Foxp3 (show FOXP3 ELISA Kits)+ T cells via regulation of HIF-1a (show HIF1A ELISA Kits) pathway
Deletion of the Vhl gene causes sympathoadrenal cell death and impairs chemoreceptor-mediated adaptation to hypoxia.
Molecular dynamics of hif-1alpha (show HIF1A ELISA Kits) and VHL may determine the success of antineoplastic strategies in hypoxia-reoxygenation as predicted by computational modeling.
Loss of Vhl in adult joint cartilage is associated with earlier dysregulation of cartilage homeostasis, characterized by increased chondrocyte apoptosis, compromised chondrocyte autophagy and accelerated age-related and surgery-induced OA development.
Both Vhl and Bap1 (show BAP1 ELISA Kits) are required for kidney function. Even when Vhl is inactivated in multipotent nephron progenitor cells, Vhl loss is insufficient for renal tumorigenesis.
VHL deficiency perturbs pancreas endocrine homeostasis in mice.
data suggest that the VHL-mediated signaling in osteochondral progenitor cells plays a critical role in bone remodeling at postnatal/adult stages through coupling osteogenesis and angiogenesis
These findings demonstrated that VHL and P53 (show TP53 ELISA Kits) act synergistically in the regulation of cell proliferation and apoptosis in CCRCC. Overall, VHL and P53 (show TP53 ELISA Kits) have important roles in the regulation of cell proliferation and apoptosis in CCRCC
Our aim was to identify VHL gene mutations in Argentinian patients who fulfilled the clinical criteria for type 1 VHL disease and in patients with VHL-associated manifestations. VHL mutations were detected in 16/19 (84.2%) patients in Group 1 and included: gross deletions (4/16); nonsense mutations (6/16); frameshift mutations (4/16); missense mutations (1/16); and splicing mutations (1/16). Three mutations were novel.
Mutations in the VHL gene is associated with von Hippel-Lindau syndrome.
The von Hippel-Lindau protein (pVHL) bound directly to hydroxylated Akt (show AKT1 ELISA Kits) and inhibited Akt (show AKT1 ELISA Kits) activity.
VHL-deficient renal cancer cells gain resistance to mitochondria-activating apoptosis inducers by activating AKT (show AKT1 ELISA Kits) through the IGF1R (show IGF1R ELISA Kits)-PI3K (show PIK3CA ELISA Kits) pathway
VHL promoter hypermethylation, which may play an important role in carcinogenesis of renal cell carcinoma (RCC (show XRCC1 ELISA Kits)), is significantly associated with an increased risk of RCC (show XRCC1 ELISA Kits).
VHLalpha isoform inhibits Warburg effect via modulation of PKM splicing.
The VHL short variant is involved in protein quality control during translation.
Study identified VHL as a direct target of miR (show MLXIP ELISA Kits)-101 and demonstrated that miR (show MLXIP ELISA Kits)-101 could increase HIF1alpha (show HIF1A ELISA Kits) protein levels by repressing VHL in normoxia condition.
VHL inactivation is associated with gastrointestinal stromal tumors.
Von Hippel-Lindau syndrome (VHL) is a dominantly inherited familial cancer syndrome predisposing to a variety of malignant and benign tumors. A germline mutation of this gene is the basis of familial inheritance of VHL syndrome. The protein encoded by this gene is a component of the protein complex that includes elongin B, elongin C, and cullin-2, and possesses ubiquitin ligase E3 activity. This protein is involved in the ubiquitination and degradation of hypoxia-inducible-factor (HIF), which is a transcription factor that plays a central role in the regulation of gene expression by oxygen. RNA polymerase II subunit POLR2G/RPB7 is also reported to be a target of this protein. Alternatively spliced transcript variants encoding distinct isoforms have been observed.
, von Hippel-Lindau disease tumor suppressor
, von Hippel-Lindau syndrome homolog
, von Hippel-Lindau syndrome protein homolog
, elongin binding protein
, protein G7