Apoptosis-linked gene 2-deficient mice exhibit normal T-cell development and function

Ihn Kyung Jang, Renju Hu, Emanuela Lacaná, Luciano D'Adamio, Hua Gu

Research output: Contribution to journalArticle

50 Citations (Scopus)

Abstract

The apoptosis-linked gene product, ALG-2, is a member of the family of intracellular Ca2+-binding proteins and a part of the apoptotic machinery controlled by T-cell receptor (TCR), Fas, and glucocorticoid signals. To explore the physiologic function of ALG-2 in T-cell development and function, we generated mice harboring a null mutation in the alg-2 gene. The alg-2 null mutant mice were viable and fertile and showed neither gross developmental abnormality nor immune dysfunction. Analyses of apoptotic responses of ALG-2-deficient T cells demonstrated that ALG-2 deficiency failed to block apoptosis induced by TCR, Fas, or dexamethasone signals. These findings indicate that ALG-2 is physiologically dispensable for apoptotic responses induced by the above signaling pathways and suggest that other functionally redundant proteins might exist in mammalian cells.

Original languageEnglish (US)
Pages (from-to)4094-4100
Number of pages7
JournalMolecular and Cellular Biology
Volume22
Issue number12
DOIs
StatePublished - 2002
Externally publishedYes

Fingerprint

T-Cell Antigen Receptor
Apoptosis
T-Lymphocytes
Dexamethasone
Glucocorticoids
Genes
Carrier Proteins
Mutation
Proteins

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cell Biology

Cite this

Apoptosis-linked gene 2-deficient mice exhibit normal T-cell development and function. / Jang, Ihn Kyung; Hu, Renju; Lacaná, Emanuela; D'Adamio, Luciano; Gu, Hua.

In: Molecular and Cellular Biology, Vol. 22, No. 12, 2002, p. 4094-4100.

Research output: Contribution to journalArticle

Jang, Ihn Kyung ; Hu, Renju ; Lacaná, Emanuela ; D'Adamio, Luciano ; Gu, Hua. / Apoptosis-linked gene 2-deficient mice exhibit normal T-cell development and function. In: Molecular and Cellular Biology. 2002 ; Vol. 22, No. 12. pp. 4094-4100.
@article{96c8fa96d63249aeb75209318b5de4cc,
title = "Apoptosis-linked gene 2-deficient mice exhibit normal T-cell development and function",
abstract = "The apoptosis-linked gene product, ALG-2, is a member of the family of intracellular Ca2+-binding proteins and a part of the apoptotic machinery controlled by T-cell receptor (TCR), Fas, and glucocorticoid signals. To explore the physiologic function of ALG-2 in T-cell development and function, we generated mice harboring a null mutation in the alg-2 gene. The alg-2 null mutant mice were viable and fertile and showed neither gross developmental abnormality nor immune dysfunction. Analyses of apoptotic responses of ALG-2-deficient T cells demonstrated that ALG-2 deficiency failed to block apoptosis induced by TCR, Fas, or dexamethasone signals. These findings indicate that ALG-2 is physiologically dispensable for apoptotic responses induced by the above signaling pathways and suggest that other functionally redundant proteins might exist in mammalian cells.",
author = "Jang, {Ihn Kyung} and Renju Hu and Emanuela Lacan{\'a} and Luciano D'Adamio and Hua Gu",
year = "2002",
doi = "10.1128/MCB.22.12.4094-4100.2002",
language = "English (US)",
volume = "22",
pages = "4094--4100",
journal = "Molecular and Cellular Biology",
issn = "0270-7306",
publisher = "American Society for Microbiology",
number = "12",

}

TY - JOUR

T1 - Apoptosis-linked gene 2-deficient mice exhibit normal T-cell development and function

AU - Jang, Ihn Kyung

AU - Hu, Renju

AU - Lacaná, Emanuela

AU - D'Adamio, Luciano

AU - Gu, Hua

PY - 2002

Y1 - 2002

N2 - The apoptosis-linked gene product, ALG-2, is a member of the family of intracellular Ca2+-binding proteins and a part of the apoptotic machinery controlled by T-cell receptor (TCR), Fas, and glucocorticoid signals. To explore the physiologic function of ALG-2 in T-cell development and function, we generated mice harboring a null mutation in the alg-2 gene. The alg-2 null mutant mice were viable and fertile and showed neither gross developmental abnormality nor immune dysfunction. Analyses of apoptotic responses of ALG-2-deficient T cells demonstrated that ALG-2 deficiency failed to block apoptosis induced by TCR, Fas, or dexamethasone signals. These findings indicate that ALG-2 is physiologically dispensable for apoptotic responses induced by the above signaling pathways and suggest that other functionally redundant proteins might exist in mammalian cells.

AB - The apoptosis-linked gene product, ALG-2, is a member of the family of intracellular Ca2+-binding proteins and a part of the apoptotic machinery controlled by T-cell receptor (TCR), Fas, and glucocorticoid signals. To explore the physiologic function of ALG-2 in T-cell development and function, we generated mice harboring a null mutation in the alg-2 gene. The alg-2 null mutant mice were viable and fertile and showed neither gross developmental abnormality nor immune dysfunction. Analyses of apoptotic responses of ALG-2-deficient T cells demonstrated that ALG-2 deficiency failed to block apoptosis induced by TCR, Fas, or dexamethasone signals. These findings indicate that ALG-2 is physiologically dispensable for apoptotic responses induced by the above signaling pathways and suggest that other functionally redundant proteins might exist in mammalian cells.

UR - http://www.scopus.com/inward/record.url?scp=0036258163&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036258163&partnerID=8YFLogxK

U2 - 10.1128/MCB.22.12.4094-4100.2002

DO - 10.1128/MCB.22.12.4094-4100.2002

M3 - Article

C2 - 12024023

AN - SCOPUS:0036258163

VL - 22

SP - 4094

EP - 4100

JO - Molecular and Cellular Biology

JF - Molecular and Cellular Biology

SN - 0270-7306

IS - 12

ER -