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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 Kits (10) and VHL Proteins (7) and many more products for this protein.
Showing 10 out of 113 products:
Human Monoclonal VHL Primary Antibody for IHC (f), IP - ABIN967508
Baba, Hirai, Kawakami, Kishida, Sakai, Kaneko, Yao, Shuin, Kubota, Hosaka, Ohno: Tumor suppressor protein VHL is induced at high cell density and mediates contact inhibition of cell growth. in Oncogene 2001
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Human Monoclonal VHL Primary Antibody for ELISA, WB - ABIN393528
Peña, Lathia, Shan, Escudier, Bukowski: Biomarkers predicting outcome in patients with advanced renal cell carcinoma: Results from sorafenib phase III Treatment Approaches in Renal Cancer Global Evaluation Trial. in Clinical cancer research : an official journal of the American Association for Cancer Research 2010
Show all 5 references for ABIN393528
Human Monoclonal VHL Primary Antibody for IHC (fro), IHC (p) - ABIN264443
Los, Jansen, Kaelin, Lips, Blijham, Voest: Expression pattern of the von Hippel-Lindau protein in human tissues. in Laboratory investigation; a journal of technical methods and pathology 1996
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Human Polyclonal VHL Primary Antibody for EIA, WB - ABIN453458
Olmos, Arenas, Bienes, Calzada, Aragonés, Garcia-Bermejo, Landazuri, Lucio-Cazaña: 15-Deoxy-Delta(12,14)-prostaglandin-J(2) reveals a new pVHL-independent, lysosomal-dependent mechanism of HIF-1alpha degradation. in Cellular and molecular life sciences : CMLS 2009
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Human Polyclonal VHL Primary Antibody for EIA, WB - ABIN453457
Hatzimichael, Dranitsaris, Dasoula, Benetatos, Stebbing, Crook, Bourantas: Von Hippel-Lindau methylation status in patients with multiple myeloma: a potential predictive factor for the development of bone disease. in Clinical lymphoma & myeloma 2009
Show all 3 references for ABIN453457
Human Polyclonal VHL Primary Antibody for ELISA, WB - ABIN185675
Kong, Lin, Liang, Fath, Sang, Caro: Histone deacetylase inhibitors induce VHL and ubiquitin-independent proteasomal degradation of hypoxia-inducible factor 1alpha. in Molecular and cellular biology 2006
Human Monoclonal VHL Primary Antibody for EIA, IHC (p) - ABIN121157
Staller, Sulitkova, Lisztwan, Moch, Oakeley, Krek: Chemokine receptor CXCR4 downregulated by von Hippel-Lindau tumour suppressor pVHL. in Nature 2003
Human Polyclonal VHL Primary Antibody for IHC, ELISA - ABIN1533202
Latif, Tory, Gnarra, Yao, Duh, Orcutt, Stackhouse, Kuzmin, Modi, Geil: Identification of the von Hippel-Lindau disease tumor suppressor gene. in Science (New York, N.Y.) 1993
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 Antibodies).
Vhl and Kif3a (show KIF3A Antibodies) deletion accelerates renal cyst formation
maintains the stability and suppressive function of Foxp3 (show FOXP3 Antibodies)+ T cells via regulation of HIF-1a (show HIF1A Antibodies) pathway
Deletion of the Vhl gene causes sympathoadrenal cell death and impairs chemoreceptor-mediated adaptation to hypoxia.
Molecular dynamics of hif-1alpha (show HIF1A Antibodies) 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 Antibodies) 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 Antibodies) act synergistically in the regulation of cell proliferation and apoptosis in CCRCC. Overall, VHL and P53 (show TP53 Antibodies) 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 (show VHLL Antibodies) (pVHL) bound directly to hydroxylated Akt (show AKT1 Antibodies) and inhibited Akt (show AKT1 Antibodies) activity.
VHL-deficient renal cancer cells gain resistance to mitochondria-activating apoptosis inducers by activating AKT (show AKT1 Antibodies) through the IGF1R (show IGF1R Antibodies)-PI3K (show PIK3CA Antibodies) pathway
VHL promoter hypermethylation, which may play an important role in carcinogenesis of renal cell carcinoma (show MOK Antibodies) (RCC (show XRCC1 Antibodies)), is significantly associated with an increased risk of RCC (show XRCC1 Antibodies).
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 Antibodies)-101 and demonstrated that miR (show MLXIP Antibodies)-101 could increase HIF1alpha (show HIF1A Antibodies) 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