Interaction between fortilin and transforming growth factor-beta stimulated clone-22 (TSC-22) prevents apoptosis via the destabilization of TSC-22

Jeong Heon Lee, Seung Bae Rho, Sang Yoon Park, Taehoon Chun

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

Yeast two-hybrid screening was conducted using a human ovary cDNA library to search for a novel binding protein using transforming growth factor-beta stimulated clone-22 (TSC-22). The selected protein was fortilin, which has been characterized as a nuclear anti-apoptotic protein. Overexpression of fortilin in ovarian carcinoma cells reversed TSC-22-mediated apoptosis, and the inhibition of fortilin expression via small interfering RNA (siRNA) resulted in an increase in the apoptosis of ovarian carcinoma cells. Moreover, fortilin overexpression promoted the degradation of TSC-22. Thus, an interaction between fortilin and TSC-22 prevents apoptosis via the destabilization of TSC-22 in ovarian carcinoma cells. Structured summary: MINT-6173230, MINT-6173253:TSC22 (uniprotkb:Q15714) physically interacts (MI:0218) with fortilin (uniprotkb:P13693) by co-immunoprecipitation (MI:0019)MINT-6173217:TSC22 (uniprotkb:Q15714) binds (MI:0407) fortilin (uniprotkb:P13693) by pull-down (MI:0096)MINT-6173240, MINT-6173270:TSC22 (uniprotkb:Q15714) physically interacts (MI:0218) with fortilin (uniprotkb:P13693) by two-hybrid (MI:0018).

Original languageEnglish
Pages (from-to)1210-1218
Number of pages9
JournalFEBS Letters
Volume582
Issue number8
DOIs
Publication statusPublished - 2008 Apr 9

Fingerprint

Transforming Growth Factor beta
Clone Cells
Cells
Apoptosis
Carcinoma
Apoptosis Regulatory Proteins
Nuclear Proteins
Gene Library
Immunoprecipitation
Yeast
Small Interfering RNA
Ovary
Carrier Proteins
Screening
Yeasts
Degradation
Proteins

Keywords

  • Apoptosis
  • Fortilin
  • Ovarian carcinoma cell
  • TSC-22
  • Yeast two hybrid

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

Interaction between fortilin and transforming growth factor-beta stimulated clone-22 (TSC-22) prevents apoptosis via the destabilization of TSC-22. / Lee, Jeong Heon; Rho, Seung Bae; Park, Sang Yoon; Chun, Taehoon.

In: FEBS Letters, Vol. 582, No. 8, 09.04.2008, p. 1210-1218.

Research output: Contribution to journalArticle

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abstract = "Yeast two-hybrid screening was conducted using a human ovary cDNA library to search for a novel binding protein using transforming growth factor-beta stimulated clone-22 (TSC-22). The selected protein was fortilin, which has been characterized as a nuclear anti-apoptotic protein. Overexpression of fortilin in ovarian carcinoma cells reversed TSC-22-mediated apoptosis, and the inhibition of fortilin expression via small interfering RNA (siRNA) resulted in an increase in the apoptosis of ovarian carcinoma cells. Moreover, fortilin overexpression promoted the degradation of TSC-22. Thus, an interaction between fortilin and TSC-22 prevents apoptosis via the destabilization of TSC-22 in ovarian carcinoma cells. Structured summary: MINT-6173230, MINT-6173253:TSC22 (uniprotkb:Q15714) physically interacts (MI:0218) with fortilin (uniprotkb:P13693) by co-immunoprecipitation (MI:0019)MINT-6173217:TSC22 (uniprotkb:Q15714) binds (MI:0407) fortilin (uniprotkb:P13693) by pull-down (MI:0096)MINT-6173240, MINT-6173270:TSC22 (uniprotkb:Q15714) physically interacts (MI:0218) with fortilin (uniprotkb:P13693) by two-hybrid (MI:0018).",
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AU - Rho, Seung Bae

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AU - Chun, Taehoon

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N2 - Yeast two-hybrid screening was conducted using a human ovary cDNA library to search for a novel binding protein using transforming growth factor-beta stimulated clone-22 (TSC-22). The selected protein was fortilin, which has been characterized as a nuclear anti-apoptotic protein. Overexpression of fortilin in ovarian carcinoma cells reversed TSC-22-mediated apoptosis, and the inhibition of fortilin expression via small interfering RNA (siRNA) resulted in an increase in the apoptosis of ovarian carcinoma cells. Moreover, fortilin overexpression promoted the degradation of TSC-22. Thus, an interaction between fortilin and TSC-22 prevents apoptosis via the destabilization of TSC-22 in ovarian carcinoma cells. Structured summary: MINT-6173230, MINT-6173253:TSC22 (uniprotkb:Q15714) physically interacts (MI:0218) with fortilin (uniprotkb:P13693) by co-immunoprecipitation (MI:0019)MINT-6173217:TSC22 (uniprotkb:Q15714) binds (MI:0407) fortilin (uniprotkb:P13693) by pull-down (MI:0096)MINT-6173240, MINT-6173270:TSC22 (uniprotkb:Q15714) physically interacts (MI:0218) with fortilin (uniprotkb:P13693) by two-hybrid (MI:0018).

AB - Yeast two-hybrid screening was conducted using a human ovary cDNA library to search for a novel binding protein using transforming growth factor-beta stimulated clone-22 (TSC-22). The selected protein was fortilin, which has been characterized as a nuclear anti-apoptotic protein. Overexpression of fortilin in ovarian carcinoma cells reversed TSC-22-mediated apoptosis, and the inhibition of fortilin expression via small interfering RNA (siRNA) resulted in an increase in the apoptosis of ovarian carcinoma cells. Moreover, fortilin overexpression promoted the degradation of TSC-22. Thus, an interaction between fortilin and TSC-22 prevents apoptosis via the destabilization of TSC-22 in ovarian carcinoma cells. Structured summary: MINT-6173230, MINT-6173253:TSC22 (uniprotkb:Q15714) physically interacts (MI:0218) with fortilin (uniprotkb:P13693) by co-immunoprecipitation (MI:0019)MINT-6173217:TSC22 (uniprotkb:Q15714) binds (MI:0407) fortilin (uniprotkb:P13693) by pull-down (MI:0096)MINT-6173240, MINT-6173270:TSC22 (uniprotkb:Q15714) physically interacts (MI:0218) with fortilin (uniprotkb:P13693) by two-hybrid (MI:0018).

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