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By screening a rat liver cDNA library, Duan et al. The human and rat proteins had molecular masses of 28 and 21 kD, respectively.
They also analyzed a variety of fetal tissues for levels of the 2 VHL isoforms, isoform I, which contains all 3 exons, and isoform II, which contains only exons 1 and 3.
Although VHL expression was found to be ubiquitous, particularly high levels of expression were detected in the urogenital system, brain, spinal cord, sensory ganglia, eyes, and bronchial epithelium.
Both isoforms of VHL were detected in all tissues, and the ratio of isoforms was similar between tissues. They showed that this kD protein is initiated from the second translation start site at codon 54, which contains a more conserved Kozak consensus sequence and thus may serve as a second, internal, translation initiation site.
The significance of a second translation start site is underscored by the lack of mutations found between the first and second methionine codons of the VHL gene in both sporadic and VHL-associated renal carcinomas.
This observation suggested that mutation in this region may not lead to VHL inactivation if translation could be initiated at the second methionine codon, producing a functional VHL protein.
Furthermore, both the rat and mouse contain only 19 of the 53 amino acids present in this region in the human VHL ORF.
VHL30 resides primarily in the cytosol, with lower amounts found in the nucleus or associated with cell membranes. In contrast, VHL19 is equally distributed between the nucleus and cytosol and is not found in association with membranes.
Thus, cells contain 2 biologically active VHL gene products. In silico analysis identified binding sites for numerous transcription factors within the conserved regions, and deletion analysis of the promoter in a reporter assay in and HeLa cells identified 1 negative and 2 positive regulatory elements.
The curves for tumors in VHL syndrome were compatible with a single mutation model, whereas the age incidence curves for sporadic tumors suggested a 2-stage mutation process.
On the whole, the findings suggested that the VHL gene functions as a recessive tumor suppressor gene. Studies of loss of heterozygosity LOH showed that in 7 tumors from 7 familial cases in which the parental origin of the 3pp25 allele loss could be determined, the allele had been lost from the chromosome inherited from the unaffected parent.
When expressed in COS-7 cells, Duan et al. A complicated pattern of cellular proteins was seen that could be specifically coimmunoprecipitated with the introduced VHL protein.
A complex containing VHL and proteins with apparent molecular masses of 16 and 9 kD was the most consistently observed. Certain naturally occurring VHL missense mutations demonstrated either complete or partial loss of the pp9 complex.
They suggested that VHL may execute its function via formation of specific multiprotein complexes. Vogelstein referred to the VHL gene as a gatekeeper gene for cancers such as those of the kidney.
Rubenstein and Yaari suggested that the VHL gene may serve that role in relation to astrocytoma. They presented the pedigree of a Puerto Rican family in which at least 9 members had von Hippel-Lindau syndrome and 2 of these had astrocytoma.
To elucidate the biochemical mechanisms underlying tumor suppression by the VHL protein, Duan et al. They found that 2 transcriptional elongation factors, elongin B and elongin C , bind in vitro and in vivo to a short, colinear region of the VHL protein that is frequently mutated in human tumors.
The results were interpreted as indicating that the normal tumor suppression function of VHL protein involves the inhibition of transcription elongation by its binding to elongin B and elongin C.
In a review article, Tyers and Willems stated that the VHL protein is part of a complex that includes elongin B, elongin C, and cullin-2 CUL2; , proteins that are associated with transcriptional elongation and ubiquitination.
Both SCF and APC interact with a set of adaptor proteins that recruit different binding partners through specific protein-protein interaction domains.
Mutation or deletion of this domain is associated with VHL syndrome, and 2 mutations that disrupt the normal interaction with TRiC and impair VHL folding were identified.
These results defined a novel role for TRiC in mediating oligomerization and suggested that inactivating mutations can impair polypeptide function by interfering with chaperone-mediated folding.
In densely grown cells, it is predominantly in the cytoplasm, whereas in sparse cultures, most of the protein can be detected in the nucleus.
They identified a putative nuclear localization signal in the first 60 and first 28 amino acids of the human and rat VHL protein, respectively.
Sequences in the C-terminal region of VHL protein may also be required for localization to the cytosol.
The findings indicated a novel cell-density-dependent pathway responsible for the regulation of VHL cellular localization. Reintroduction of wildtype, but not mutant, VHL into these cells had no demonstrable effect on their growth in vitro but inhibited their ability to form tumors in nude mice.
Like many cancer cells, the RCC fails to exit the cell cycle upon serum withdrawal. The cyclin-dependent kinase inhibitor p27 CDKN1B; accumulates upon serum withdrawal, only in the presence of VHL, as a result of an increase in protein stability.
Thus, VHL appears to be the first tumor suppressor involved in the regulation of cell cycle exit, which is consistent with its gatekeeper function in the kidney.
To discover genes involved in VHL-mediated carcinogenesis, Ivanov et al. Large-scale RNA differential display technology applied to these cell lines identified several differentially expressed genes, including an alpha carbonic anhydrase gene, termed CA12 The deduced protein sequence was classified as a one-pass transmembrane carbonic anhydrase possessing an apparently intact catalytic domain in the extracellular CA module.
Reintroduced wildtype VHL strongly inhibited the overexpression of the CA12 gene in the parental renal cell carcinoma cell lines. Similar results were obtained with CA9 which encodes another transmembrane carbonic anhydrase with an intact catalytic domain.
Although both domains of the VHL protein contributed to regulation of CA12 expression, the elongin binding domain alone could effectively regulate CA9 expression.
By fluorescence in situ hybridization, Ivanov et al. Moreover, upon genotoxic stress, VHL invoked an interaction between p53 and p EP; and the acetylation of p53, which led to an increase in p53 transcriptional activity and cell cycle arrest and apoptosis.
Overexpression of Daam2 in 2 mouse models of malignant glioma also resulted in accelerated tumorigenesis.
Protein screening and bioinformatic analysis revealed an inverse correlation of DAAM2 and VHL expression across a broad spectrum of cancers.
Similarly, Vhl protein expression was reduced in Daam2 gain-of-function mouse tumors and increased in Daam2 loss-of-function mouse tumors.
Gene expression analysis showed altered Vhl signaling in Daam2-expressing mouse gliomas. Reintroduction of wildtype, but not mutant, VHL protein into these cells specifically inhibited production of these mRNAs under normoxic conditions, thus restoring their previously described hypoxia-inducible profile.
Using a VEGF promoter-luciferase construct for cotransfection with a wildtype VHL vector in embryonic kidney and renal cell carcinoma cell lines, they showed that wildtype VHL protein inhibited VEGF promoter activity in a dose-dependent manner up to 5- to fold.
This VHL-responsive element is GC rich and specifically bound the transcription factor Sp1 in crude nuclear extracts.
They further demonstrated that VHL and Sp1 directly interact with an inhibitory effect on Sp1, suggesting that loss of Sp1 inhibition may be important in the pathogenesis of von Hippel-Lindau syndrome and renal cell carcinoma.
Eleven genes encoding products involved in glucose transport, glycolysis, high energy phosphate metabolism, and angiogenesis were examined; 9 were induced by hypoxia in other mammalian cells and 2 were repressed by hypoxia.
None of these responses were seen in the VHL-defective cell lines. Responses to hypoxia were restored by stable transfection of a wildtype VHL gene, with effects ranging from a modest action of hypoxia to substantial regulation.
These results indicated that the previously described upregulation of hypoxia-inducible mRNAs in VHL-defective cells extend to a broad range of oxygen-regulated genes and involves a constitutive 'hypoxia pattern' for both positively and negatively regulated genes.
Hypoxia-inducible factor-1 HIF1; has a key role in cellular response to hypoxia, including the regulation of genes involved in energy metabolism, angiogenesis, and apoptosis.
The alpha subunits of HIF are rapidly degraded by the proteasome under normal conditions but are stabilized by hypoxia.
Cobaltous ions or iron chelators mimic hypoxia, indicating that the stimuli may interact through effects on a ferroprotein oxygen sensor. Reexpression of VHL restored oxygen-dependent instability.
These findings indicated that the interaction between HIF1 and VHL is iron dependent and that it is necessary for the oxygen-dependent degradation of HIF-alpha subunits.
Because proline hydroxylation requires molecular oxygen and iron, this protein modification may play a key role in mammalian oxygen sensing.
An absolute requirement for dioxygen as a cosubstrate and iron as a cofactor suggests that HIF-PH functions directly as a cellular oxygen sensor.
In mammalian cells, they showed that the HIF-prolyl hydroxylases are represented by 3 proteins, PHD1 , PHD2 , and PHD3 , with a conserved 2-histidinecarboxylate iron coordination motif at the catalytic site.
Direct modulation of recombinant enzyme activity by graded hypoxia, iron chelation, and cobaltous ions mirrored the characteristics of HIF induction in vivo, fulfilling requirements for these enzymes being oxygen sensors that regulate HIF.
Furthermore, leu to val LV; Mutations causing HAB susceptibility types 1, 2A, and 2B demonstrated variable effects on HIF-alpha subunit and elongin binding, but all resulted in defective HIF-alpha regulation and loss of fibronectin binding.
These studies strengthened the notion that HIF deregulation plays a causal role in hemangioblastoma and renal carcinoma, and raised the possibility that abnormal fibronectin matrix assembly contributes to pheochromocytoma pathogenesis in the setting of VHL syndrome.
Hemangioblastomas of the central nervous system and retina in VHL patients overexpress vascular endothelial growth factor, which represents a potential target for anti-angiogenic drugs.
Hematocrit was normal before the beginning of the trial, and no progression of hemangioblastomas was observed. Polycythemia had never been reported in SU trials for advanced malignancies.
In the studies of Richard et al. An analysis of clear cell renal carcinoma that manifests mutations in the VHL gene in most cases revealed an association of strong CXCR4 expression with poor tumor-specific survival.
To identify novel target genes of the VHL protein, Zatyka et al. Expression array analysis identified 9 genes that demonstrated a greater than 2-fold decrease in expression in both RCC cell lines after restoration of wildtype VHL protein.
Homozygous disruption of the Vhl gene in mice results in embryonic lethality from lack of placental vasculogenesis Gnarra et al. To investigate Vhl function in the adult, Haase et al.
They showed that mice heterozygous for the 1-lox allele developed cavernous hemangiomas of the liver, a rare manifestation in the human disease.
Histologically, these tumors were associated with hepatocellular steatosis and focal proliferations of small vessels. To study the cellular origin of these lesions, Haase et al.
Deletion of VHL in the liver resulted in severe steatosis, many blood-filled vascular cavities, and foci of increased vascularization within the hepatic parenchyma.
These histopathologic changes were similar to those seen in livers from mice heterozygous for the 1-lox allele. Hypoxia-inducible mRNAs encoding vascular endothelial growth factor, glucose transporter-1, and erythropoietin EPO; were upregulated.
Thus, targeted inactivation of mouse Vhl replicated clinical features of the human disease and underscored the importance of the VHL gene product in the regulation of hypoxia-responsive genes in vivo.
In contrast, mice lacking Hif1a in osteoblasts had long bones that were significantly thinner and less vascularized than those of controls.
Loss of Vhl in osteoblasts increased endothelial sprouting from the embryonic metatarsals in vitro but had little effect on osteoblast function in the absence of blood vessels.
Endocytosis plays a major role in the deactivation of receptors localized to the plasma membrane, and early endocytic events require the small GTPase RAB5 and its effector rabaptin-5 RABEP1; Primary kidney and breast tumors with strong hypoxic signatures showed significantly lower expression of rabaptin-5 RNA and protein.
VHL1 and HIF1 control longevity by a mechanism distinct from both dietary restriction and insulin-like signaling. Immunofluorescence and biochemical fractionation experiments showed that fibronectin colocalized with a fraction of VHL associated with the endoplasmic reticulum, and cold competition experiments suggested that complexes between fibronectin and VHL protein exist in intact cells.
Both the microtubule binding and stabilization functions depended on amino acids , a hotspot for mutations in VHL syndrome. They found that the syndrome-associated mutations Y98H Using immunofluorescence and confocal microscopy, Lolkema et al.
Cilia were absent in renal cell carcinoma cells derived from a VHL patient, but reintroduction of VHL into these cells resulted in rapid cilia assembly.
The cilia function of VHL required residues 1 to 53, which constitute an acidic domain, and residues 95 to , which were previously implicated in microtubule binding and tumor suppression.
They showed that expression of the VHL protein is correlated with neuronal differentiation but not with glial differentiation in CNS progenitor cells, and also that VHL gene transduction induces neuronal differentiation.
The hydroxyproline inserts into a gap in the VHL hydrophobic core, at a site that is a hotspot for tumorigenic mutations, with its 4-hydroxyl group recognized by buried serine and histidine residues.
Although the beta sheet-like interactions contribute to the stability of the complex, the hydroxyproline contacts are central to the strict specificity characteristic of signaling.
They found that optimized hydrogen bonding to the buried hydroxyprolyl group confers precise discrimination between hydroxylated and unmodified prolyl residues.
Using restriction fragment analysis, Latif et al. Eighteen of these rearrangements were due to deletion in the candidate gene.
Using pulsed field gel electrophoresis and cosmid mapping, Latif et al. Using single-strand conformation polymorphism and heteroduplex analysis to investigate 94 VHL patients without large deletions, Crossey et al.
The 2 most frequent mutations were argto-gln In addition, a search for EcoRI rearrangements revealed germline anomalies in 5 patients. The 61 variants could be subdivided into 20 mutations predicted to alter the open reading frame and 43 DNA sequence variants that on a priori grounds were of unknown biologic consequence.
A similar screening in 18 patients with sporadic hemangioblastoma revealed 2 missense DNA variants. All of the tumors showed distinct 'second-hit' point mutations on the wildtype allele, even those tumors originating in the same patient.
Moreover, the same types of tumors from the same locations also showed different point mutations. Using markers specific for chromosome 3, Glasker et al.
The tumors consisted of 3 central nervous system hemangioblastomas, 7 renal cell carcinomas, 3 cystic renal structures, 2 pancreatic tumors, and 1 pancreatic cyst.
Deletion size was highly variable, ranging from short deletions around the VHL gene to complete deletion of chromosome 3.
However, there was no correlation between deletion size and site of the germline mutation, affected organ, or type or biological behavior of the tumor.
The Knudson model predicts that sporadic cancers should be associated with mutations in the same locus affected in the corresponding hereditary cancer.
In 4 of them, the pattern was due to small, 1- to nucleotide deletions that created frameshift mutations and, presumably, truncated proteins.
Two mutations were somatic and 2 were germline. In a mother and 2 sons with pheochromocytoma, Crossey et al. None of them had evidence of VHL syndrome.
No allelic loss was shown in colon adenomas from 8 informative patients. The authors suggested that VHL gene loss may represent a relatively late event in colonic neoplasia progression.
Seven tumors had a frameshift mutation due either to deletion of 1 or more basepairs 6 cases or to insertion of 1 basepair 1 case.
The remaining 3 tumors had either point mutations with intron splice site sequences 2 cases or a point mutation resulting in an amino acid substitution 1 case.
Evidence for germline alterations of the VHL gene was found in 2 patients who showed identical mutations in both tumors and corresponding leukocyte DNA.
The non-germline mutations included tumors from individuals 70, 62, 60, 55, and 52 years old. Evidence of mutation of the VHL gene was associated exclusively with nonpapillary renal cell carcinoma.
Fearon reviewed more than 20 different hereditary cancer syndromes that had been defined and attributed to specific germline mutations in various inherited cancer genes.
In a useful diagram, he illustrated the roles of allelic variation '1 gene - different syndromes' and genetic heterogeneity 'different genes - 1 syndrome' in inherited cancer syndromes.
VHL mutations were used as an example of the former: Van der Harst et al. This was undertaken to follow up on the work of Neumann et al.
They found mutations in the VHL gene in 8 patients; 2 patients were an uncle and nephew who had the same missense mutation, R64P In 4 other patients, missense mutations, P25L, L63P In 2 other cases, the mutations were located not in the coding region but in the intronic sequence but not within splice sites , adjacent to the exon, so that they were probably not related to the syndrome.
The results suggested that 8. They detected an abnormal SSCP pattern in 73 samples. VHL mutations were found only in the nonpapillary renal cell carcinoma subtype, as previously reported.
To compare somatic and germline mutations, they used the VHL database, which included mutations. The study of mutational events revealed a significant difference between somatic and germline mutations.
This pattern corresponds to mutations leading to truncated proteins, with few specific missense mutations. For comparison, they performed the same analyses in 17 sporadic pheochromocytomas.
In patients receiving dialysis, Yoshida et al. No mutations were found in the tyrosine kinase domain of the MET oncogene, where mutations had previously been found in cases of papillary RCCs.
They retrospectively evaluated patients from 55 families with large germline VHL deletions, including 42 intragenic partial deletions and 13 complete VHL deletions.
An age-adjusted comparison demonstrated a higher prevalence of RCC in patients with partial germline VHL deletions relative to complete deletions In the group with missense mutations, Gallou et al.
Inheritance of germline mutations in both VHL alleles was found by Ang et al. The VHL protein plays an important role in hypoxia sensing.
It binds to hydroxylated HIF1-alpha and serves as a recognition component of an E3 ubiquitin ligase complex.
Two Danish sibs and an American boy were homozygous for the RW mutation Additionally, a Croatian boy was homozygous for an HD mutation They found that up to half of the consecutive patients with apparent congenital erythrocytosis and increased serum EPO whom they had examined had mutations of both VHL alleles.
They concluded that VHL mutations are the most frequent cause of recessive congenital erythrocytosis and define a class of disorders due to augmented hypoxia sensing.
Human and Drosophila TRC8 proteins localize to the endoplasmic reticulum. Loss of either Drosophila Trc8 or Vhl resulted in an identical ventral midline defect.
Direct interaction between Trc8 and Vhl in Drosophila was confirmed by GST-pull-down and coimmunoprecipitation experiments.
At about 4 weeks of age, the mice developed rapidly progressive renal disease with hematuria, proteinuria, and renal failure with crescentic glomerulonephritis with prominent segmental fibrin deposition and fibrinoid necrosis.
No immune deposits were present; the phenotype was similar to human 'pauci-immune' rapidly progressive glomerulonephritis RPGN.
Treatment of the mice with a Cxcr4 antibody resulted in clinical improvement, and isolated overexpression of Cxcr4 was sufficient to cause glomerular disease.
Although bone marrow cellularity and morphology was similar to controls, spleens from the mutant mice showed increased numbers of erythroid progenitors and megakaryocytes, as well as erythroid differentiation of splenic cells in vitro.
Using immunofluorescence microscopy, Zehetner et al. Conditional inactivation of Vhl in beta cells promoted a diversion of glucose away from mitochondria into lactate production, causing cells to produce high levels of glycolytically derived ATP and to secrete elevated levels of insulin at low glucose concentrations.
Vhl deletion was associated with upregulation of Hif1a and the glucose transporter Glut1, an Hif1a target gene. Combined deletion of Vhl and Hif1a rescued the defects due to Vhl deletion alone, implying that they resulted from Hif1a activation.
Mutant cells had preserved regulation of both HIF-alpha factors with slightly greater normotoxic dysregulation of HIF2-alpha.
RQ-derived teratomas had a growth advantage and showed hemangioma formation. Homozygous mice were embryonic lethal due to placental failure, and heterozygous mice developed renal cysts and were predisposed to the carcinogen-promoted renal carcinoma.
In a patient with von Hippel-Lindau syndrome , Latif et al. Following the revised codon numbering system of Kuzmin et al.
In a cell line from a sporadic case of renal cell carcinoma , Latif et al.
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