Interaction of p107 with Cyclin A Independent of Complex Formation with Viral Oncoproteins

Ewen, Mark E.; Faha, Barbara; Harlow, Ed; Livingston, David M.

doi:10.1126/science.1532457

Cited by 216 publications

(140 citation statements)

References 28 publications

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“…It is well established that DNA tumor antigens can interact with components of the cell cycle regulatory apparatus (Giordano et al 1989(Giordano et al , 1991Tsai et al 1991;Ewen et al 1992;). Thus, we were particularly interested in the study of fibroblasts that are transformed by means other than DNA tumor viruses.…”

Section: Discussionmentioning

confidence: 99%

“…Cyclin A and CDK2 have been found to form a quaternary complex with a retinoblastoma gene product (Rb 1)-related protein (p107) and the transcription factor E2F in a cell cycleregulated manner, suggesting that cyclin A-CDK2 kinase might be controlling gene expression during G1 and S phase of the cell cycle (Cao et al 1992;Devoto et al 1992;Ewen et al 1992;Pagano et al 1992b;Shirodkar et al 1992; for review, see Nevins 1992). Similarly, cyclin E was also found to form a quaternary complex with CDK2, p107, and E2F but in a temporally distinct manner from the cyclin A quaternary complex (Lees et al 1992).…”

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confidence: 99%

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Subunit rearrangement of the cyclin-dependent kinases is associated with cellular transformation.

Xiong¹,

Zhang²,

Beach³

1993

Genes Dev.

476

325

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Subunit rearrangement of the cyclin-dependent kinases is associated with cellular transformation.

Xiong¹,

Zhang²,

Beach³

1993

Genes Dev.

476

325

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“…The spacer region has a different sequence, which renders unique each member of the retinoblastoma family. The spacer region is dispensable for pRb/p105 function, whereas this region is more conserved between p107 and pRb2/ p130 and mediates their interaction with specific cyclin/ cdk complexes (Ewen et al, 1992;Adams et al, 1996;Lacy and Whyte, 1997).…”

Section: Rb1: the Gene And The Protein Structurementioning

confidence: 99%

pRb2/p130: a new candidate for retinoblastoma tumor formation

Falco

Giordano

2006

Oncogene

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Retinoblastoma is the most common primary intraocular tumor in childhood. Mutations in both the alleles of the RB1 gene represent the causative agent for the tumor to occur. It is becoming evident that, although these alterations represent key events in the genesis of retinoblastoma, they are not sufficient per se for the tumor to develop, and other additional genetic or epigenetic alterations must occur. A supportive role in the genesis of retinoblastoma has recently been proposed for the RB1-related gene RB2/ p130. Additionally, several other genetic alterations involving different chromosomes have been described as relevant in the tumorigenic process. In this review we will analyse current knowledge about the molecular mechanisms involved in retinoblastoma, paying particular attention to the mechanisms of inactivation of the biological function of the retinoblastoma family of proteins.

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“…6 Once the cell progresses toward the G1-S border, cyclin E is degraded and cyclin A enters into a complex with cdk2, hence triggering S-phase entry. 7 Several potent protein inhibitors of cyclin-cdk complexes are implicated in regulating kinase activity. p21 is expressed during all phases of the cell cycle and may be induced when quiescent cells are stimulated to proliferate.…”

mentioning

confidence: 99%

Different Cell Cycle Regulation of Vascular Smooth Muscle in Genetic Hypertension

Tanner

Greutert²,

Barandier³

et al. 2003

Hypertension

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Abstract-Vascular smooth muscle cells (VSMC) from spontaneously hypertensive rats (SHR) proliferate faster than those from Wistar-Kyoto rats (WKY). Therefore regulation of cell cycle progression was examined in VSMC from both strains. Analysis of G1 progression was performed in VSMC synchronized by serum starvation. Double staining for propidium iodide and bromodeoxyuridine revealed that G1 progression was faster in SHR as compared with WKY. Indeed, 59Ϯ6% of VSMC from SHR but only 14Ϯ10% of those from WKY had left G1 phase after 24 hours of mitogenic stimulation. Moreover, 15Ϯ2% of SHR cells had already completed the cycle at this time point. Western blot analysis demonstrated that the level of cyclin D, cyclin E, and cyclin A was higher in SHR cells progressing through G1 phase, whereas expression of cyclin-dependent kinase 2 as well as the cyclin-dependent kinase inhibitors p21 and p27 were similar in the two groups. Consistent with a higher level of cyclins, the activity of cyclin-dependent kinase 2 was more pronounced in SHR cells. Analysis of G2 progression was performed in VSMC synchronized by treatment with aphidicolin and revealed an additional difference in cell cycle regulation between SHR and WKY. Indeed, the level of cell division cycle kinase 2 was higher in cells from SHR, whereas that of its catalytic partner cyclin B was similar. Consistent with this pattern of expression, the activity of cell division cycle kinase 2 was more pronounced in VSMC from SHR as compared with WKY. Thus, these data demonstrate that the different proliferation of VSMC from SHR and WKY is related to a different progression in G1 phase as the result of the expression of cyclin D, cyclin A, and cyclin E as well as a different progression in G2 phase caused by expression of cell division cycle kinase 2. Key Words: rats, spontaneously hypertensive Ⅲ muscle, smooth, vascular Ⅲ hypertension, genetic Ⅲ molecular biology V ascular smooth muscle cell (VSMC) proliferation contributes to the arterial remodeling occurring in hypertension. 1 Indeed, VSMC from spontaneously hypertensive rats (SHR) proliferate faster as compared with normotensive control rats (Wistar-Kyoto rats; WKY). 2 This difference has been attributed to cyclin-dependent kinase II activity. 3,4 A detailed analysis of cell cycle regulation in SHR as compared with WKY, however, has not been performed yet.Cell cycle progression is determined by formation of protein complexes between cyclins and cyclin-dependent kinases (cdk), which depends on the cell cycle-regulated expression of cyclins assembling with preexisting cdk. 5 Cyclin D associates with cdk2, cdk4, and cdk6 and is important for early G1 progression, whereas cyclin E associates primarily with cdk2 and promotes late G1 progression. 6 Once the cell progresses toward the G1-S border, cyclin E is degraded and cyclin A enters into a complex with cdk2, hence triggering S-phase entry. 7 Several potent protein inhibitors of cyclin-cdk complexes are implicated in regulating kinase activity. p21 is expressed during all...

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Interaction of p107 with Cyclin A Independent of Complex Formation with Viral Oncoproteins

Cited by 216 publications

References 28 publications

Subunit rearrangement of the cyclin-dependent kinases is associated with cellular transformation.

Subunit rearrangement of the cyclin-dependent kinases is associated with cellular transformation.

pRb2/p130: a new candidate for retinoblastoma tumor formation

Different Cell Cycle Regulation of Vascular Smooth Muscle in Genetic Hypertension

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