Loss of von Hippel-Lindau protein causes cell density dependent deregulation of CyclinD1 expression through hypoxia-inducible factor. (Q44790615)

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3 November 2019

title

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

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3 November 2019

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15

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3 November 2019

Masaya Baba

1

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3 November 2019

11

Noboru Nakaigawa

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3 November 2019

author name string

Syuiohi Hirai

2

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3 November 2019

Hisafumi Yamada-Okabe

3

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3 November 2019

Kenji Hamada

4

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3 November 2019

Hisahiro Tabuchi

5

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3 November 2019

Kazuki Kobayashi

6

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3 November 2019

Keiichi Kondo

7

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3 November 2019

Minoru Yoshida

8

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3 November 2019

Akio Yamashita

9

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3 November 2019

Takeshi Kishida

10

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3 November 2019

Youji Nagashima

12

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3 November 2019

Yoshinobu Kubota

13

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3 November 2019

Masahiro Yao

14

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3 November 2019

language of work or name

English

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publication date

1 May 2003

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3 November 2019

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3 November 2019

volume

22

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3 November 2019

issue

18

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3 November 2019

page(s)

2728-2738

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https://scigraph.springernature.com/pub.10.1038/sj.onc.1206373

3 November 2019

exact match

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Negative regulation of hypoxia-inducible genes by the von Hippel-Lindau protein

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Down-regulation of transmembrane carbonic anhydrases in renal cell carcinoma cell lines by wild-type von Hippel-Lindau transgenes

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Cyclin D1 expression is regulated positively by the p42/p44MAPK and negatively by the p38/HOGMAPK pathway.

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HIF activation identifies early lesions in VHL kidneys: evidence for site-specific tumor suppressor function in the nephron

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Colony-stimulating factor 1 regulates novel cyclins during the G1 phase of the cell cycle

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

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Measurement of cell numbers in microtiter culture plates using the fluorescent dye Hoechst 33258.

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The von Hippel-Lindau tumor-suppressor gene product forms a stable complex with human CUL-2, a member of the Cdc53 family of proteins

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Reduced skin tumor development in cyclin D1-deficient mice highlights the oncogenic ras pathway in vivo

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