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2007 | 54 | 3 |

Tytuł artykułu

Overexpression of BimSs3, the novel isoform of Bim, can trigger cell apoptosis by inducing cytochrome c release from mitochondria

Warianty tytułu

Języki publikacji

EN

Abstrakty

EN
Bim is defined as the pro-apoptotic BH3-only protein of the Bcl-2 family, which is a critical sensor and mediator in the mitochondrial-dependent apoptosis. In a previous work, we have cloned a novel transcript of Bim (GenBank accession number: AY305716) from the fetal brain cDNA, which is widely expressed in some carcinoma tissues and normal human tissues. According to the sequence analysis and the newly-defined nomenclature system of Bim isoforms (Adachi et al., 2005, Cell Death Differ 2: 192), we term it BimSs3 according to its characteristic structure. The subcellular location analysis indicated that the fused protein GFP-BimSs3 is distributed in the whole cell, mainly to the nucleus. Overexpression of BimSs3 in HEK293 cells causes apoptosis (28.16 ± 1.55%) compared to the negative control (5.44 ± 2.63%). It also causes cytochrome c release from the mitochondrial fraction to the cytosolic fraction during apoptosis. Western blotting assay indicates the molecular mass of GFP-BimSs3 is approximately 31.0 kDa (GFP: 27 kDa). Hence the open reading frame of BimSs3 may initiate at the second ATG and encodes a 36 amino-acid peptide with BH3 domain.

Wydawca

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Rocznik

Tom

54

Numer

3

Opis fizyczny

p.603-610,fig.,ref.

Twórcy

autor
  • Fudan University, Shanghai, P.R.China
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Bibliografia

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  • Chen D, Zhou Q (2004) Caspase cleavage of BimEL triggers a positive feedback amplification of apoptotic signaling. Proc Natl Acad Sci 5: 1235–1240.
  • Chen JZ, Ji CN, Gu SH, Li JX, Zhao EP, Huang Y, Huang L, Ying K, Xie Y, Mao YM (2004) Over-expression of Bim alpha3, a novel isoform of human Bim, result in cell apoptosis. Int J Biochem Cell Biol 8: 1554–1561.
  • Chen L, Willis SN, Wei A, Smith BJ, Fletcher JI, Hinds MG, Colman PM, Day CL, Adams JM, Huang DC (2005) Differential targeting of prosurvival Bcl-2 proteins by their BH3-only ligands allows complementary apoptotic function. Mol Cell 3: 393–403.
  • Cheng EH, Wei MC, Weiler S, Flavell RA, Mak TW, Lindsten T, Korsmeyer SJ (2001) BCL-2, BCL-X(L) sequester BH3 domain-only molecules preventing BAX- and BAK-mediated mitochondrial apoptosis. Mol Cell 3: 705–711.
  • Cory S, Huang DC, Adams JM (2003) The Bcl-2 family: roles in cell survival and oncogenesis. Oncogene 53: 8590–8607.
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  • Letai A, Bassik MC, Walensky LD, Sorcinelli MD, Weiler S, Korsmeyer SJ (2002) Distinct BH3 domains either sensitize or activate mitochondrial apoptosis, serving as prototype cancer therapeutics. Cancer Cell 2: 183–192.
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  • Wakabayashi T (1999) Structural changes of mitochondria related to apoptosis: swelling and megamitochondria formation. Acta Biochim Polon 46: 223–237.
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  • Willis SN, Adams JM (2005) Life in the balance: how BH3–only proteins induce apoptosis. Curr Opin Cell Biol 6: 617–625.
  • Zhang J, Chen J, Liu L, Ji C, Gu S, Ying K, Mao Y (2006) Different gene expression profiles of AD293 and HEK293 cell lines that show contrasting susceptibility to apoptosis induced by overexpression of Bim L. Acta Biochim Polon 53: 525–530.
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Typ dokumentu

Bibliografia

Identyfikatory

Identyfikator YADDA

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