Cdks, cyclins and CKIs : Roles beyond cell cycle regulation
(2013) In Development (Cambridge) 140(15). p.3079-3093- Abstract
Cyclin-dependent kinases (Cdks) are serine/threonine kinases and their catalytic activities are modulated by interactions with cyclins and Cdk inhibitors (CKIs). Close cooperation between this trio is necessary for ensuring orderly progression through the cell cycle. In addition to their well-established function in cell cycle control, it is becoming increasingly apparent that mammalian Cdks, cyclins and CKIs play indispensable roles in processes such as transcription, epigenetic regulation, metabolism, stem cell self-renewal, neuronal functions and spermatogenesis. Even more remarkably, they can accomplish some of these tasks individually, without the need for Cdk/cyclin complex formation or kinase activity. In this Review, we discuss... (More)
Cyclin-dependent kinases (Cdks) are serine/threonine kinases and their catalytic activities are modulated by interactions with cyclins and Cdk inhibitors (CKIs). Close cooperation between this trio is necessary for ensuring orderly progression through the cell cycle. In addition to their well-established function in cell cycle control, it is becoming increasingly apparent that mammalian Cdks, cyclins and CKIs play indispensable roles in processes such as transcription, epigenetic regulation, metabolism, stem cell self-renewal, neuronal functions and spermatogenesis. Even more remarkably, they can accomplish some of these tasks individually, without the need for Cdk/cyclin complex formation or kinase activity. In this Review, we discuss the latest revelations about Cdks, cyclins and CKIs with the goal of showcasing their functional diversity beyond cell cycle regulation and their impact on development and disease in mammals.
(Less)
- author
- Lim, Shuhui
and Kaldis, Philipp
LU
- publishing date
- 2013-08-01
- type
- Contribution to journal
- publication status
- published
- keywords
- Cdk, Cki, Cyclin, Dna damage repair, Epigenetic regulation, Metabolism, Neuronal functions, Proteolytic degradation, Spermatogenesis, Stem cell self-renewal, Transcription
- in
- Development (Cambridge)
- volume
- 140
- issue
- 15
- pages
- 15 pages
- publisher
- The Company of Biologists Ltd
- external identifiers
-
- pmid:23861057
- scopus:84880264045
- ISSN
- 0950-1991
- DOI
- 10.1242/dev.091744
- language
- English
- LU publication?
- no
- id
- 948a2c18-3829-496c-9a5d-273861ec10e2
- date added to LUP
- 2019-09-18 13:57:20
- date last changed
- 2024-07-10 02:49:30
@article{948a2c18-3829-496c-9a5d-273861ec10e2, abstract = {{<p>Cyclin-dependent kinases (Cdks) are serine/threonine kinases and their catalytic activities are modulated by interactions with cyclins and Cdk inhibitors (CKIs). Close cooperation between this trio is necessary for ensuring orderly progression through the cell cycle. In addition to their well-established function in cell cycle control, it is becoming increasingly apparent that mammalian Cdks, cyclins and CKIs play indispensable roles in processes such as transcription, epigenetic regulation, metabolism, stem cell self-renewal, neuronal functions and spermatogenesis. Even more remarkably, they can accomplish some of these tasks individually, without the need for Cdk/cyclin complex formation or kinase activity. In this Review, we discuss the latest revelations about Cdks, cyclins and CKIs with the goal of showcasing their functional diversity beyond cell cycle regulation and their impact on development and disease in mammals.</p>}}, author = {{Lim, Shuhui and Kaldis, Philipp}}, issn = {{0950-1991}}, keywords = {{Cdk; Cki; Cyclin; Dna damage repair; Epigenetic regulation; Metabolism; Neuronal functions; Proteolytic degradation; Spermatogenesis; Stem cell self-renewal; Transcription}}, language = {{eng}}, month = {{08}}, number = {{15}}, pages = {{3079--3093}}, publisher = {{The Company of Biologists Ltd}}, series = {{Development (Cambridge)}}, title = {{Cdks, cyclins and CKIs : Roles beyond cell cycle regulation}}, url = {{http://dx.doi.org/10.1242/dev.091744}}, doi = {{10.1242/dev.091744}}, volume = {{140}}, year = {{2013}}, }