Cdc2 and Cdk2 Kinase Activated by Transforming Growth Factor-β1 Trigger Apoptosis through the Phosphorylation of Retinoblastoma Protein in FaO Hepatoma Cells

Choi, Kyeong Sook; Eom, Young Woo; Kang, Yup; Ha, Mahn Joon; Rhee, Horace; Yoon, Ji‐Won; Kim, Seong‐Jin

doi:10.1074/jbc.274.45.31775

Cited by 72 publications

(55 citation statements)

References 61 publications

(57 reference statements)

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“…For example, dysregulation of the components of the cell cycle machinery (leading to an aberrant cell cycle) has been reported to be one of the most potent stimuli for induction of apoptosis [23]. Unscheduled activation of Cdk molecules can induce apoptosis in several experimental settings, while inhibition of Cdk activity protects cells against apoptosis [24][25][26]. However, it is widely known that many chemotherapeutic drugs inhibit the activities of Cdks, leading to eventual cell death [27].…”

Section: Discussionmentioning

confidence: 99%

Cdc2 and Cdk2 play critical roles in low dose doxorubicin-induced cell death through mitotic catastrophe but not in high dose doxorubicin-induced apoptosis

Park

Eom

Choi

2005

Biochemical and Biophysical Research Communications

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Section: Discussionmentioning

confidence: 99%

Cdc2 and Cdk2 play critical roles in low dose doxorubicin-induced cell death through mitotic catastrophe but not in high dose doxorubicin-induced apoptosis

Park

Eom

Choi

2005

Biochemical and Biophysical Research Communications

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“…Previous studies suggest that the production of reactive oxygen intermediates (Sa´nchez et al, 1996;Atfi et al, 1997) and the activation of caspase-family proteases (Chen and Chang, 1997;Inayat-Hussain et al, 1997) are involved in TGF-b-induced apoptosis. In addition, pRb (Choi et al, 1999) and Bcl-2 (Lafon et al, 1996) have been suggested to regulate TGF-b-induced apoptosis. More recently, it has been reported that TGF-b can generate apoptosis indirectly by inducing the expression of the connective tissue growth factor (Hishikawa et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

RGD peptides released from βig-h3, a TGF-β-induced cell-adhesive molecule, mediate apoptosis

Kim

Jeong

et al. 2003

Oncogene

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big-h3 is a transforming growth factor-b (TGF-b)-induced cell-adhesive molecule and has an RGD sequence at its Cterminus. A previous report suggested that big-h3 normally undergoes carboxy-terminal processing that results in the loss of the RGD sequence. RGD peptides appear to play various roles in cell function. Here we show that the RGD peptides released from big-h3 may facilitate TGF-b-induced apoptosis. We found that carboxy-terminal cleavage of big-h3 occurred after its secretion, and that overexpression of the wild-type big-h3 induced apoptosis, unlike the C-terminal deleted but RGDcontaining mutant big-h3, which is resistant to C-terminal processing. The big-h3-induced apoptosis was abolished by either deletion of the RGD sequence or mutation of RGD to RAE. Synthetic peptides of ERGDEL and GRGDSP derived from big-h3 and fibronectin, respectively, also induced apoptosis, unlike ERGEEL and GRGESP. Culture supernatants of cells overexpressing big-h3 filtered to isolate molecules smaller than 3 kDa also induced apoptosis. A fusion protein composed of the N-terminal 100 amino acids of fibronectin and the RGDcontaining C-terminal part of big-h3 was also subjected to C-terminal cleavage and overexpression resulted in apoptosis. The anti-big-h3 antibody blocks TGF-binduced apoptosis. Thus, big-h3 may be important in regulating cell apoptosis by providing soluble RGD peptides.

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“…Apoptosis can be blocked in certain models of cultured human and murine cell lines by chemical inhibitors of CDKs, such as roscovitine (De Luca et al, 1997;Choi et al, 1999;Hsu et al, 1999) and structurally related purine type compounds such as olomoucine (Hsu et al, 1999) and purvalanol (Adachi et al, 2001) or a flavonoid compound, flavopiridol (Park et al, 1996). Despite their chemical diversity, these small molecules bind to the ATP-binding pocket of the catalytic domain and reduce the activity of the enzyme (Vesely et al, 1994;Knockaert et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Analysis of cyclin B1 and CDK activity during apoptosis induced by camptothecin treatment

et al. 2006

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We have studied the role of cyclins and cyclin-dependent kinase (CDK) activity in apoptosis induced by camptothecin (CPT). In this model, 22% of the cells stain for annexin-V at 24 h and then proceed to be 93% positive by 72 h. This time window permits the analysis of cyclins in cells that are committed to apoptosis but not yet dead. We provide evidence that cyclin protein levels and then associated kinase levels increase after CPT treatment. Strikingly, cyclin B1 and cyclin E1 proteins are present at the same time in CPT treated HT29 cells. Although cyclin B1 and E1 CDK complexes are activated in CPT treated cells, only the cyclin B1 complex is required for apoptosis since reduction of cyclin B1 by RNAi or roscovitine treatment reduces the number of annexin-V-stained cells. We have detected poorly organized chromosomes and phosphorylated histone H3 epitopes at the time of maximum cyclin B1/CDK kinase activity in CPT-treated cells, which suggests that these cells enter a mitotic catastrophe. Understanding which CDKs are required for apoptosis may allow us to better adapt CDK inhibitors for use as anti-cancer compounds.

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Cdc2 and Cdk2 Kinase Activated by Transforming Growth Factor-β1 Trigger Apoptosis through the Phosphorylation of Retinoblastoma Protein in FaO Hepatoma Cells

Cited by 72 publications

References 61 publications

Cdc2 and Cdk2 play critical roles in low dose doxorubicin-induced cell death through mitotic catastrophe but not in high dose doxorubicin-induced apoptosis

Cdc2 and Cdk2 play critical roles in low dose doxorubicin-induced cell death through mitotic catastrophe but not in high dose doxorubicin-induced apoptosis

RGD peptides released from βig-h3, a TGF-β-induced cell-adhesive molecule, mediate apoptosis

Analysis of cyclin B1 and CDK activity during apoptosis induced by camptothecin treatment

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