Concomitant deregulation of HIF1alpha and cell cycle proteins in VHL-mutated renal cell carcinomas. (Q53668297)

17 May 2018

title

Concomitant deregulation of HIF1alpha and cell cycle proteins in VHL-mutated renal cell carcinomas. (English)

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17 May 2018

6

Hiltrud Brauch

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17 May 2018

Derek John Atkins

1

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17 May 2018

Christian Gingert

2

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17 May 2018

Christina Justenhoven

3

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17 May 2018

Gerd Emil Schmahl

4

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17 May 2018

Marcellus Stephanus Bonato

5

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17 May 2018

Stephan Störkel

7

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17 May 2018

publication date

1 July 2005

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17 May 2018

published in

Virchows Archiv

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17 May 2018

volume

447

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17 May 2018

issue

3

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17 May 2018

page(s)

634-642

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17 May 2018

https://scigraph.springernature.com/pub.10.1007/s00428-005-1262-y

exact match

0 references

cites work

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The tumour suppressor protein VHL targets hypoxia-inducible factors for oxygen-dependent proteolysis

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Loss of von Hippel-Lindau protein causes cell density dependent deregulation of CyclinD1 expression through hypoxia-inducible factor.

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Targeting of HIF-alpha to the von Hippel-Lindau ubiquitylation complex by O2-regulated prolyl hydroxylation

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Germline mutations in the Von Hippel-Lindau disease (VHL) gene in families from North America, Europe, and Japan

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Histopathology and classification of renal cell tumors (adenomas, oncocytomas and carcinomas). The basic cytological and histopathological elements and their use for diagnostics

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Identification of cyclin D1 and other novel targets for the von Hippel-Lindau tumor suppressor gene by expression array analysis and investigation of cyclin D1 genotype as a modifier in von Hippel-Lindau disease.

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Constitutive activation of hypoxia-inducible genes related to overexpression of hypoxia-inducible factor-1alpha in clear cell renal carcinomas

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The von Hippel-Lindau tumor suppressor gene is required for cell cycle exit upon serum withdrawal

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VHL alterations in human clear cell renal cell carcinoma: association with advanced tumor stage and a novel hot spot mutation

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Mutations of the VHL tumour suppressor gene in renal carcinoma

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Hypoxia inducible factor activates the transforming growth factor-alpha/epidermal growth factor receptor growth stimulatory pathway in VHL(-/-) renal cell carcinoma cells

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Hypoxia-inducible factor 1alpha is essential for cell cycle arrest during hypoxia

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VHL mutations and their correlation with tumour cell proliferation, microvessel density, and patient prognosis in clear cell renal cell carcinoma

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HIF-1, O(2), and the 3 PHDs: how animal cells signal hypoxia to the nucleus

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The von Hippel-Lindau tumor suppressor protein is required for proper assembly of an extracellular fibronectin matrix

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NF-kappaB and cell-cycle regulation: the cyclin connection

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Transforming growth factor alpha is a target for the von Hippel-Lindau tumor suppressor

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Loss of heterozygosity occurs centromeric to RB without associated abnormalities in the retinoblastoma gene in tumors from patients with metastatic renal cell carcinoma.

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Hypoxia inhibits G1/S transition through regulation of p27 expression

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Retinoblastoma protein in human renal cell carcinoma in relation to alterations in G1/S regulatory proteins

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NF-kappaB plays a key role in hypoxia-inducible factor-1-regulated erythropoietin gene expression

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HIF-1 in cell cycle regulation, apoptosis, and tumor progression

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The Rb/E2F pathway and cancer

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The role of HIF-1 alpha in transcriptional regulation of the proximal tubular epithelial cell response to hypoxia

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10.1007/S00428-005-1262-Y

Identifiers

DOI

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17 May 2018

PubMed ID

15991006

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17 May 2018