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

doi:10.1016/j.febslet.2008.01.066

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

Department of Biotechnology

Research output: Contribution to journal › Article › peer-review

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 language	English
Pages (from-to)	1210-1218
Number of pages	9
Journal	FEBS Letters
Volume	582
Issue number	8
DOIs	https://doi.org/10.1016/j.febslet.2008.01.066
Publication status	Published - 2008 Apr 9

Keywords

Apoptosis
Fortilin
Ovarian carcinoma cell
TSC-22
Yeast two hybrid

ASJC Scopus subject areas

Biophysics
Structural Biology
Biochemistry
Molecular Biology
Genetics
Cell Biology

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@article{e862e4217a494ff18d623717fc17647c,

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

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).",

keywords = "Apoptosis, Fortilin, Ovarian carcinoma cell, TSC-22, Yeast two hybrid",

author = "Lee, {Jeong Heon} and Rho, {Seung Bae} and Park, {Sang Yoon} and Taehoon Chun",

note = "Funding Information: This work was supported by a grant from the Korea Health 21 R&D Project, Ministry of Health & Welfare, Republic of Korea (Project Number: A040004) and by a grant from the National Cancer Center, Korea (NCC-0510571-3).",

year = "2008",

month = apr,

day = "9",

doi = "10.1016/j.febslet.2008.01.066",

language = "English",

volume = "582",

pages = "1210--1218",

journal = "FEBS Letters",

issn = "0014-5793",

publisher = "Elsevier",

number = "8",

}

TY - JOUR

T1 - Interaction between fortilin and transforming growth factor-beta stimulated clone-22 (TSC-22) prevents apoptosis via the destabilization of TSC-22

AU - Lee, Jeong Heon

AU - Rho, Seung Bae

AU - Park, Sang Yoon

AU - Chun, Taehoon

N1 - Funding Information: This work was supported by a grant from the Korea Health 21 R&D Project, Ministry of Health & Welfare, Republic of Korea (Project Number: A040004) and by a grant from the National Cancer Center, Korea (NCC-0510571-3).

PY - 2008/4/9

Y1 - 2008/4/9

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).

KW - Apoptosis

KW - Fortilin

KW - Ovarian carcinoma cell

KW - TSC-22

KW - Yeast two hybrid

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U2 - 10.1016/j.febslet.2008.01.066

DO - 10.1016/j.febslet.2008.01.066

M3 - Article

C2 - 18325344

AN - SCOPUS:41149096388

VL - 582

SP - 1210

EP - 1218

JO - FEBS Letters

JF - FEBS Letters

SN - 0014-5793

IS - 8

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