抄録
Caspases and Bcl-xL, the mammalian homologues of the Caenorhabditis elegans (C. elegans) ced-3 and ced-9 genes, respectively, regulate apoptosis of various cells. Caspase-3 is processed into an active form (p20 or p17 and p12) during apoptosis. We investigated the relation between caspase-3 and Bcl-xL during development by examining activation of caspase-3 and apoptotic cells in Bcl-x-deficient (bcl-x(-/-)) mice at embryonic (E) day 11.5. We used a double-staining technique with a cleavage site-directed antibody against caspase-3 (anti-p20/17) and terminal-deoxytransferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL). Bcl-xL-deficiency increased both numbers of p20/17-positive and -negative apoptotic cells in dorsal root ganglia (DRG); the numbers of p20/17-positive apoptotic cells in the caudal parts of the ventral hindbrain and ventral spinal cord; and the numbers of p20/17-negative apoptotic cells in the dorsal midbrain, dorsal hindbrain, and dorsal spinal cord. Thus, Bcl-xL blocks the caspase-3-dependent apoptotic pathway in the restricted regions of the nervous system during development. Furthermore, these observations suggest that Bcl-xL protects against activation of the caspase-3-independent apoptotic pathway. Other caspases or apoptotic mechanisms may also be activated in the nervous systems of bcl-x(-/-) mice. Copyright (C) 1999 Elsevier Science B.V.
| 元の言語 | 英語 |
|---|---|
| ページ（範囲） | 69-78 |
| ページ数 | 10 |
| ジャーナル | Developmental Brain Research |
| 巻 | 116 |
| 発行部数 | 1 |
| DOI | |
| 出版物ステータス | 出版済み - 8 5 1999 |
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All Science Journal Classification (ASJC) codes
- Developmental Neuroscience
- Developmental Biology
これを引用
Bcl-xL is a negative regulator of caspase-3 activation in immature neurons during development. / Urase, Koko; Momoi, Takashi; Fujita, Eriko; Isahara, Kyoko; Uchiyama, Yasuo; Tokunaga, Akinori; Nakayama, Kei Ichi; Motoyama, Noboru.
：: Developmental Brain Research, 巻 116, 番号 1, 05.08.1999, p. 69-78.研究成果: ジャーナルへの寄稿 › 記事
}
TY - JOUR
T1 - Bcl-xL is a negative regulator of caspase-3 activation in immature neurons during development
AU - Urase, Koko
AU - Momoi, Takashi
AU - Fujita, Eriko
AU - Isahara, Kyoko
AU - Uchiyama, Yasuo
AU - Tokunaga, Akinori
AU - Nakayama, Kei Ichi
AU - Motoyama, Noboru
PY - 1999/8/5
Y1 - 1999/8/5
N2 - Caspases and Bcl-xL, the mammalian homologues of the Caenorhabditis elegans (C. elegans) ced-3 and ced-9 genes, respectively, regulate apoptosis of various cells. Caspase-3 is processed into an active form (p20 or p17 and p12) during apoptosis. We investigated the relation between caspase-3 and Bcl-xL during development by examining activation of caspase-3 and apoptotic cells in Bcl-x-deficient (bcl-x(-/-)) mice at embryonic (E) day 11.5. We used a double-staining technique with a cleavage site-directed antibody against caspase-3 (anti-p20/17) and terminal-deoxytransferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL). Bcl-xL-deficiency increased both numbers of p20/17-positive and -negative apoptotic cells in dorsal root ganglia (DRG); the numbers of p20/17-positive apoptotic cells in the caudal parts of the ventral hindbrain and ventral spinal cord; and the numbers of p20/17-negative apoptotic cells in the dorsal midbrain, dorsal hindbrain, and dorsal spinal cord. Thus, Bcl-xL blocks the caspase-3-dependent apoptotic pathway in the restricted regions of the nervous system during development. Furthermore, these observations suggest that Bcl-xL protects against activation of the caspase-3-independent apoptotic pathway. Other caspases or apoptotic mechanisms may also be activated in the nervous systems of bcl-x(-/-) mice. Copyright (C) 1999 Elsevier Science B.V.
AB - Caspases and Bcl-xL, the mammalian homologues of the Caenorhabditis elegans (C. elegans) ced-3 and ced-9 genes, respectively, regulate apoptosis of various cells. Caspase-3 is processed into an active form (p20 or p17 and p12) during apoptosis. We investigated the relation between caspase-3 and Bcl-xL during development by examining activation of caspase-3 and apoptotic cells in Bcl-x-deficient (bcl-x(-/-)) mice at embryonic (E) day 11.5. We used a double-staining technique with a cleavage site-directed antibody against caspase-3 (anti-p20/17) and terminal-deoxytransferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL). Bcl-xL-deficiency increased both numbers of p20/17-positive and -negative apoptotic cells in dorsal root ganglia (DRG); the numbers of p20/17-positive apoptotic cells in the caudal parts of the ventral hindbrain and ventral spinal cord; and the numbers of p20/17-negative apoptotic cells in the dorsal midbrain, dorsal hindbrain, and dorsal spinal cord. Thus, Bcl-xL blocks the caspase-3-dependent apoptotic pathway in the restricted regions of the nervous system during development. Furthermore, these observations suggest that Bcl-xL protects against activation of the caspase-3-independent apoptotic pathway. Other caspases or apoptotic mechanisms may also be activated in the nervous systems of bcl-x(-/-) mice. Copyright (C) 1999 Elsevier Science B.V.
UR - http://www.scopus.com/inward/record.url?scp=0032773486&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0032773486&partnerID=8YFLogxK
U2 - 10.1016/S0165-3806(99)00076-0
DO - 10.1016/S0165-3806(99)00076-0
M3 - Article
C2 - 10446348
AN - SCOPUS:0032773486
VL - 116
SP - 69
EP - 78
JO - Developmental Brain Research
JF - Developmental Brain Research
SN - 0165-3806
IS - 1
ER -