Cell-cycle inhibition by independent CDK and PCNA binding domains in p21 super cip1

Article Abstract:

The cyclin-dependent kinases (CDK) and proliferating cell nuclear antigen (PCNA) inhibitory activities of p21 is functionally independent and resides in separate protein domains from p27 and p57. p21, p27 and p57 belongs to a family of proteins that bind to and inhibit CDK required for initiation of S phase. The PCNA and CDK inhibitory and binding activities of p21 respectively resides in the C-terminal domain and N-terminal domain. p21 can inhibit cell-cycle progression by two separate stoichiometric mechanisms and their effectiveness in inhibition is dependent on the relative abundance of CDKs and PCNA.

Observations, Antineoplastic agents, Cell cycle, Antimitotic agents

---

Mechanism of CDK activation revealed by the structure of a cyclinA-CDK2 complex

Article Abstract:

CyclinA's involvement in the activation of the catalytic cyclin-dependent kinase (CDK) can be better understood through the determination of the crystal structure of human cyclinA-cyclin-dependent kinase (CDK)2-ATP complex. The determination reveals that cyclin binding causes conformational changes in the active site of CDK2 that are probably responsible for the activity. The alpha 1 helix of CDK2, which contains the PSTAIRE sequence found in cyclin-dependent kinases, rotates about its axis and the T-loop of CDK2 also moves, removing the blockade to the catalytic site, for phosphorylation to proceed.

Research, Protein kinases, Structure-activity relationships (Biochemistry)

---

Mutations increasing autoinhibition inactivate tumour supressors Smad2 and Smad4

Article Abstract:

Tumour-suppressor proteins Smad2 and Smad4 inhibit growth when stimulated by the growth factor TGF-beta. The inhibitory function of the N domain involves interaction the C domain that stops the association of Smad2 with Smad4, and this is particularly increased in tumour-derived forms of Smad 2 and four. Mutations in the C domain upset the effector functions of the Smad proteins. However N-domain arginine mutations inhibit Smad signalling via autoinhibitory functions.

Tumors

Similar abstracts:

• Abstracts: Modification by nuclear export? Structure of the DNA-binding domains from NFAT, Fos and Jun bound specifically to DNA
• Abstracts: Multi-scale roost-site selection by evening bats on pine-dominated landscapes in Southwest Georgia. Summer habitat use and home range analysis of the endangered Indiana bat
• Abstracts: Assessment of pre-laying motivation in the domestic hen using social interaction. Social inhibition of movement in domestic hens
• Abstracts: A prophet in his own land. Science and peace. Science in an era of political change
• Abstracts: Activation of postsynaptically silent synapses during pairing-induced LTP in CA1 region of hippocampal slice. Properties of synaptic transmission at single hippocampal synaptic boutons

This website is not affiliated with document authors or copyright owners. This page is provided for informational purposes only. Unintentional errors are possible.