Quinase dependente de ciclina: Diferenzas entre revisións
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==== RINGO/Speedy ====
Proteins with no homology to the cyclin family can be direct activators of CDKs.<ref name = "ringo">Mouron, Silvana; de Carcer, Guillermo; Seco, Esther; Fernandez-Miranda, Gonzalo; Malumbres, Marcos; Nebreda, Angel. (2010). "RINGO C is required to sustain the spindle assembly checkpoint." ''Journal of Cell Science.'' 123:2586-2595.</ref> One family of such activators is the RINGO/Speedy family,<ref name = "ringo" /> which was originally discovered in Xenopus. All five members discovered so far directly activate Cdk1 and Cdk2, but the RINGO/Speedy-CDK2 complex recognizes different substrates than cyclin A-CDK2 complex.<ref name = "noncyclin" />
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== Historia==
[[Leland H. Hartwell]], [[R. Timothy Hunt]], e [[Paul M. Nurse]] recibiron o [[Premio Nobel de Medicina ou Fisioloxía]] de 2001 pola completa descrición que fixeron das [[ciclina]]s e mecanismos das quinases depenentes de ciclinas, que son básicos para a regulación do ciclo celular.
== Importancia médica ==
As CDKs
▲CDKs are considered a potential target for anti-cancer medication. If it is possible to selectively interrupt the cell cycle regulation in cancer cells by interfering with CDK action, the cell will die. At present, some [[CDK inhibitor]]s such as [[seliciclib]] are undergoing clinical trials. Although it was originally developed as a potential anti-cancer drug, seliciclib has also proven to induce [[apoptosis]] in [[neutrophil granulocytes]], which mediate [[inflammation]].<ref>Rossi, Adriano G.; Sawatzky, Deborah A.; Walker, Annemieke; Ward, Carol; Sheldrake, Tara A.; Riley, Nicola A.; Caldicott, Alison; Martinez-Losa, Magdalena; Walker, Trevor R.; Duffin, Roger; Gray, Mohini; Crescenzi, Elvira; Martin, Morag C.; Brady, Hugh J; Savill, John S.; Dransfield, Ian & Haslett, Christopher (2006): Cyclin-dependent kinase inhibitors enhance the resolution of inflammation by promoting inflammatory cell apoptosis. ''Nature Medicine'' '''12''' (in print). {{DOI|10.1038/nm1468}}</ref> This means that novel drugs for treatment of [[chronic (medicine)|chronic]] inflammation diseases such as [[arthritis]] and [[cystic fibrosis]] could be developed.
Porén, cómpre facer máis investigacións porque a alteración da vía mediada polas CDK ten potencialmente graves consecuencias; aínda que os inhibidores das CDKs parecen prometedores, debe determinarse como se poden limitar os efectos secundarios para que só sexan afectadas as células diana. Como este tipo de doenzas son xeralmente tratadas con [[glicocorticoide]]s, os cales teñen graves efectos secundarios tamén, incluso un éxito menor dos novos fármacos podería ser un avance.
▲Flavopiridol ([[alvocidib]]) is the first CDK inhibitor to be tested in clinical trials after being identified in an anti-cancer agent screen in 1992. It competes for the ATP site of the CDKs.<ref>Senderowicz, AM. “Flavopiridol: the first cyclin-dependent kinase inhibitor in human clinical trials” “Invest New Drugs” 17(3):313-20</ref>
'''Táboa 4:''' Fármacos inhibidores das quinases dependentes de ciclina <ref name = "Sausville" />
▲Complications of developing a CDK drug include the fact that many CDKs are not involved in the cell cycle, but other processes such as transcription, neural physiology, and glucose homeostasis.<ref name = "Sausville">Sausville, Edward A. (2002) “Complexities in the development of cyclin-dependent kinase inhibitor drugs” “Trends in Molecular Medicine” 8:S32-S37</ref>
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| Paullones || 1, 2, 5
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|[[Seliciclib]] ||?
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== Notas ==
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