Changes in Cyclin Dependent Kinase Expression and Activity Accompanying Lens Fiber Cell Differentiation

Gao, Chun; Rampalli, Anuradha M.; Cai, Huicong; He, Hongchao; Zelenka, Peggy S.

doi:10.1006/exer.1999.0749

Cited by 45 publications

(23 citation statements)

References 57 publications

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“…The realization that the expression of p35 is not strictly limited to neuronal cells (22)(23)(24)(25)(26)(27)(28)(29) opened new lines of investigation into the mechanistic basis of terminal differentiation. On the basis of the postulated existence of a common neurohematopoietic stem cell (37,38), we conducted several studies that establish that Cdk5, activated by the so-called "p35 neuron-specific Cdk5 activator, p35Nck5a," plays a role in monocytic differentiation, both in normal human hematopoiesis and in human leukemia cells induced to differentiate to the monocytic phenotype by 1,25D 3 (26 -29).…”

Section: Discussionmentioning

confidence: 99%

“…There are ϳ2 dozen proteins with diverse functions that have been identified as Cdk5 substrates, and in neurons, this kinase has been implicated in the regulation of microtubule stability and transport, axon guidance, secretion, membrane transport, and dopamine signaling (17)(18)(19)(20)(21). Recently, several groups, including ours, have demonstrated that Cdk5 also plays an important role in nonneuronal cells and is involved in myogenesis, lens differentiation, spermatogenesis, insulin secretion, and hematopoietic cell differentiation (22)(23)(24)(25)(26)(27)(28)(29).…”

Section: Introductionmentioning

confidence: 99%

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Up-Regulation of Egr1 by 1,25-Dihydroxyvitamin D3 Contributes to Increased Expression of p35 Activator of Cyclin-Dependent Kinase 5 and Consequent Onset of the Terminal Phase of HL60 Cell Differentiation

Chen¹,

Wang²,

Wang³

et al. 2004

Cancer Research

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Up-Regulation of Egr1 by 1,25-Dihydroxyvitamin D3 Contributes to Increased Expression of p35 Activator of Cyclin-Dependent Kinase 5 and Consequent Onset of the Terminal Phase of HL60 Cell Differentiation

Chen¹,

Wang²,

Wang³

et al. 2004

Cancer Research

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“…The p57 Kip2 transcript may be evidenced in skeletal muscle, brain, heart, lung, kidney, pancreas, testis, and placenta. p57 Kip2 participates in lens-fiber differentiation (69,70) and maturation of the nervous system (71). The protein regulates neuronal migration in mouse cortex and rat neurogenesis (72,73).…”

Section: P57 Kip2 Metabolismmentioning

confidence: 99%

p57Kip2 and Cancer: Time for a Critical Appraisal

Borriello

Caldarelli

Bencivenga

et al. 2011

Molecular Cancer Research

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p57Kip2 is a cyclin-dependent kinase inhibitor belonging to the Cip/Kip family, which also includes p21Cip1 and p27Kip1. So far, p57Kip2 is the least-studied Cip/Kip protein, and for a long time its relevance has been related mainly to its unique role in embryogenesis. Moreover, genetic and molecular studies on animal models and patients with Beckwith-Wiedemann syndrome have shown that alterations in CDKN1C (the p57Kip2 encoding gene) have functional relevance in the pathogenesis of this disease. Recently, a number of investigations have identified and characterized heretofore unexpected roles for p57Kip2. The protein appears to be critically involved in initial steps of cell and tissue differentiation, and particularly in neuronal development and erythropoiesis. Intriguingly, p27Kip1, the Cip/Kip member that is most homologous to p57Kip2, is primarily involved in the process of cell cycle exit. p57Kip2 also plays a critical role in controlling cytoskeletal organization and cell migration through its interaction with LIMK-1. Furthermore, p57Kip2 appears to modulate genome expression. Finally, accumulating evidence indicates that p57Kip2 protein is frequently downregulated in different types of human epithelial and nonepithelial cancers as a consequence of genetic and epigenetic events. In summary, the emerging picture is that several aspects of p57Kip2's functions are only poorly clarified. This review represents an appraisal of the data available on the p57Kip2 gene and protein structure, and its role in human physiology and pathology. We particularly focus our attention on p57Kip2 changes in cancers and pharmacological approaches for modulating p57Kip2 levels. Mol Cancer Res; 9(10); 1269–84. ©2011 AACR.

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“…Yet, with a few exceptions, no systematic correlation has been done with the corresponding p57 KIP2 temporal and spatial pattern of expression. p57 KIP2 cooperates with negative (p27 KIP1 ) and positive (CDK2, CDK4, cyclin D, and cyclin E) cell cycle regulators to promote lens fiber differentiation (140,143,144). Particularly, it has an opposite effect on the proliferating function of cyclin D3 (144).…”

Section: Lessons From Micementioning

confidence: 99%