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anti-Human VHL Antikörper:
anti-Mouse (Murine) VHL Antikörper:
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Human Monoclonal VHL Primary Antibody für 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
Show all 7 Pubmed References
Human Monoclonal VHL Primary Antibody für IHC (f), ICS - ABIN2689963
Chen, Kishida, Duh, Renbaum, Orcutt, Schmidt, Zbar: Suppression of growth of renal carcinoma cells by the von Hippel-Lindau tumor suppressor gene. in Cancer research 1995
Show all 6 Pubmed References
HIF-1alpha (zeige HIF1A Antikörper)/miR (zeige MLXIP Antikörper)-210 pathway is strongly activated in VHL mutated paragangliomas, weakly activated in SDHx mutated PGLs (zeige PGLS Antikörper), and not activated in VHLdel- and SDHxwt/VHLwt-PGLs (zeige PGLS Antikörper).
VHL missense mutations in the p53 (zeige TP53 Antikörper) binding domain show different effects on p53 (zeige TP53 Antikörper) signaling and HIFalpha degradation in clear cell renal cell carcinoma (zeige MOK Antikörper), enhancing tumor cell survival.
the structural model of the HIF2a (zeige EPAS1 Antikörper)-pVHL complex presented in this study enhances understanding of how HIF2a (zeige EPAS1 Antikörper) is captured by pVHL. Moreover, the important contact amino acids that we identified may be useful in the development of drugs to treat HIF2a (zeige EPAS1 Antikörper)-related diseases.
these findings demonstrate that USP9X (zeige USP9X Antikörper) is a novel regulator of Von Hippel-Lindau protein (zeige VHLL Antikörper) stability, and USP9X (zeige USP9X Antikörper) may be a therapeutic target for treatment of Von Hippel-Lindau protein (zeige VHLL Antikörper)-related tumors
To the best of our knowledge, this is the first report of the coexistence of VHL disease and CPT2 (zeige CPT2 Antikörper) deficiency in the same individual. Based on findings from animal models, the case illustrates that mutations in the VHL gene might protect against renal damage caused by CPT2 (zeige CPT2 Antikörper) gene mutations.
Our work provides the first evidence that VHL mutations positively correlate with PD-L1 (zeige CD274 Antikörper) expression in ccRCC and may influence the response to ccRCC anti-PD-L1 (zeige CD274 Antikörper)/PD-1 (zeige PDCD1 Antikörper) immunotherapy.
VHL is one of the commonly disrupted genes in patients with Sarcomatoid Renal Cell Carcinoma (zeige MOK Antikörper).
This article puts together the sequential pathogenesis of VHL mutant Clear cell renal cell carcinoma (zeige MOK Antikörper) (ccRCC) by elaborating these mechanisms and the interplay of oncogenic pathways, epigenetics, metabolism and immune evasion, with a perspective on potential therapeutic strategies.
VHL promoter region 7896829 which was hypermethylated with sunitinib treatment in metastatic clear cell renal cancer
Positive staining for pVHL was observed in cancerous areas but not in normal tissues in patients with tongue cancer
Interaction between Nm23 (zeige NME1 Antikörper) and the tumor suppressor VHL
Transgenic pVHL can fully maintain normal dVHL-HIF1-alpha (zeige HIF1A Antikörper) downstream pathways in flies.
Codepletion of Vhl with Mgr (zeige GRHL1 Antikörper) gives partial rescue of tubulin (zeige TUBB Antikörper) instability, monopolar spindle formation, and loss of centrosomes.
The results establish a developmental function of the VHL gene that is relevant to its tumor-suppressor activity.
findings reveal a second type of tracheal hypoxic response in which Sima activation conflicts with developmental tracheogenesis, and identify the dVHL and ago ubiquitin ligases as key determinants of hypoxia sensitivity in tracheal cells
the vhl(-/-) zebrafish kidney is characterized by an increased tubule diameter, disorganized cilia, the dramatic formation of cytoplasmic lipid vesicles, glycogen (zeige GYS2 Antikörper) accumulation, aberrant cell proliferation and abnormal apoptosis.
In this review, we have tried to bring together knowledge on the HIF/hypoxic signaling pathway in zebrafish, including what is known on VHL functions.
by modulating hypoxia-inducible factor activity via up-regulation of VHL, FOXO3a (zeige FOXO3 Antikörper) (foxo3b) plays an important role in survival in response to hypoxic stress.
Zebrafish embryos lacking endogenous vhl lead to defective phenotypes in the renal system that were characterized by the curved and cystic pronephric tubule or/and a cystic and malformed glomerulus.
Inhibiting PHD (zeige PDC Antikörper) or knocking down VHL rescues Methyl tert (zeige TERT Antikörper)-butyl ether induced vascular lesions.
Zebrafish vhl mutants display a marked increase in blood vessel formation throughout the embryo, and the most severe neovascularization is observed in distinct areas that overlap with high vegfa (zeige VEGFA Antikörper) mRNA expression, including the vhl mutant brain and eye.
Vhl mutants develop polycythemia with increased epo (zeige EPO Antikörper)/epor (zeige EPOR Antikörper) mRNA & erythropoietin (zeige EPO Antikörper) signaling. VHL regulates hematopoiesis & erythroid differentiation. Zebrafish vhl mutants are the 1st congenital embryonic viable systemic vertebrate animal model for VHL.
kidney-specific deletion of Vhl and Pbrm1 (zeige PBRM1 Antikörper), but not either gene alone, results in bilateral, multifocal, transplantable clear cell kidney cancers.
Codeletion of VHL together with HIF2A (zeige EPAS1 Antikörper) but not with HIF1A (zeige HIF1A Antikörper) led to apparently normal kidneys, and the animals reached normal age but were anemic because of low erythropoietin (zeige EPO Antikörper) levels. Stromal deletion of HIF2A (zeige EPAS1 Antikörper) or HIF1A (zeige HIF1A Antikörper) alone did not affect kidney development.
High VHL expression is associated with liver fibrosis.
Study demonstrated that mice with a loss of one allele of the VHL gene exhibited normal phenotypes without evidence of predisposition to the development of CNS-hemangioblastomas. Heterozygous VHL +/- mice exhibited the neuroprotective response to acute cerebral ischemia/reperfusion injury due to enhanced angiogenesis by HIF-dependent regulation and HIF-independent Twist 1 (zeige TWIST1 Antikörper) signaling.
These results support the idea that the development of a full-blown VHL disease phenotype requires inactivation of the VHL gene not only in the tumor proper, but also in the stromal compartment.
Combined deletion of Vhl, Trp53 (zeige TP53 Antikörper) and Rb1 (zeige RB1 Antikörper) specifically in renal epithelial cells in mice caused clear cell renal cell carcinoma (zeige MOK Antikörper).
pVHL has a pivotal role in bleomycin-induced pulmonary fibrosis.
These findings reveal VHL-HIF-mediated metabolic compartmentalization in the developing heart and the connection between metabolism and myocardial differentiation.
Longitudinal microcomputed tomography (muCT) imaging and histopathological analyses revealed an increased rate of cyst formation, increased proportion of cysts with proliferating cells, higher frequency of atypical cysts as well as the development of neoplasms in Vhl/Kif3a (zeige KIF3A Antikörper)/Trp53 (zeige TP53 Antikörper) mutant kidneys compared to Kif3a (zeige KIF3A Antikörper)/Trp53 (zeige TP53 Antikörper) or Vhl/Kif3a (zeige KIF3A Antikörper) mutant kidneys.
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.
elongin binding protein
, protein G7
, von Hippel-Lindau disease tumor suppressor
, von hippel lindau
, von hippel lindau protein
, von Hippel-Lindau tumor suppressor
, von Hippel-Lindau syndrome homolog
, von Hippel-Lindau syndrome protein homolog
, Von Hippel-Lindau disease tumor suppressor