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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 (113) and VHL Kits (7) and many more products for this protein.
Showing 6 out of 7 products:
Human VHL Protein expressed in Wheat germ - ABIN1325000
Kim, Lee, Jang, Yi, Kim, Han, Lee, Tong, Vincelette, Gao, Yin, Evans, Choi, Qin, Liu, Zhang, Deng, Jen, Zhang, Wang, Lou: WSB1 promotes tumor metastasis by inducing pVHL degradation. in Genes & development 2015
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 Proteins).
Vhl and Kif3a (show KIF3A Proteins) deletion accelerates renal cyst formation
maintains the stability and suppressive function of Foxp3 (show FOXP3 Proteins)+ T cells via regulation of HIF-1a (show HIF1A Proteins) pathway
Deletion of the Vhl gene causes sympathoadrenal cell death and impairs chemoreceptor-mediated adaptation to hypoxia.
Molecular dynamics of hif-1alpha (show HIF1A Proteins) 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 Proteins) 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
proteome and phospho-proteomic analysis of isogenic 786-O renal cell carcinoma (show MOK Proteins) (+/-VHL) cells to compare signatures that reflect hypoxia and/or loss of VHL protein
Pars (show EPRS Proteins) plana vitrectomy in advanced VHL eye disease can improve or preserve visual function, but postoperative progression of ocular VHL disease can be accelerated in cases where retinotomy is performed.
AR-suppressed miRNA-145 is a key player in renal cell carcinoma (show MOK Proteins) progression by regulating HIF2alpha (show EPAS1 Proteins)/VEGF (show VEGFA Proteins)/MMP9 (show MMP9 Proteins)/CCND1 (show CCND1 Proteins) expression levels, irrespective of VHL status.
VHL was shown to influence cellular metabolism through its effect on HIF proteins as well as by affecting activity of other factors.
Data indicate that mutant VHL can protect HIF1alpha (show HIF1A Proteins) from SART1 (show SART1 Proteins)-dependent degradation in normoxic conditions, but this protection is lost in hypoxic settings, favoring hypoxia-dependent ccRCC proliferation.
VHLp19 has a role for regulating EPO (show EPO Proteins) levels that VHLp30 does not have, whereas VHLp30 is really the tumor suppressor isoform.
pVHL interacts with CERKL (show CERKL Proteins) and ubiquitinates it for oxygen dependent proteasomal degradation.
APOE (show APOE Proteins), VHL and MTHFR (show MTHFR Proteins) gene polymorphisms were related to the risk of renal cell carcinoma (show MOK Proteins)
Distinct von Hippel-Lindau gene and hypoxia-regulated alterations in gene and protein expression patterns of renal cell carcinoma (show MOK Proteins) are accompanied with distinct metabolic changes.
14 (51.9%) patients had a germline mutation in the succinate dehydrogenase subunit B (show SDHB Proteins) gene (SDHB (show SDHB Proteins)), and 3 (11.1%) had mutations in the von Hippel-Lindau gene
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