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Core components of this system are cyclin-dependent kinases (CDKs) that are activated upon binding to specific cyclin proteins.
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When bound to specific cyclin partners, CDKs promote cellular progression along the cellular life-cycle.
The CDKs, proteins of 300 amino acids in length, are activated by a no covalent binding with specific cyclins triggering the transition between different phases of the cell cycle.
By binding to cyclins, Tax stabilizes the cyclin D/Cdk complex, thereby enhancing its kinase activity and leading to the hyperphosphorylation of Rb.
Upon binding to the cyclin E-CDK2 complex, p27Kip1 inhibits CDK2 activity, thereby inhibiting cell cycle progression and cell proliferation.
Nevertheless, in spite of this effect of MTA on JunD cellular contents this compound almost totally inhibited cyclin D1 expression, and our ChIP experiment showed a near complete inhibition of JunD binding to the cyclin D1 promoter.
We have identified a key molecular mechanism by which cyclin Y activates atypical cyclin-dependent kinase 16 (CDK16)/PCTAIRE-1, which involves 14-3-3 14-3-3 14-3-3clin Y through phosphorylation of two residues, namely Ser and Ser.
Non-specific binding was subtracted from total binding to obtain specific binding.
P16INK4A is a tumor suppressor protein that inhibits cyclin dependant kinases (CDK -4 or -6 binding to CDK -4 D which regulates the G1 cell cycle checkpornts [ 19, 20].
IL-7 enhanced AP-1 binding to cyclin D1 promoter, while blocking IL-7R reduced AP-1 binding to cyclin D1 promoter (Fig. 9e) in vivo.
IL-7 enhanced AP-1 binding to cyclin D1 promoter, while blocking IL-7R reduced AP-1 binding to cyclin D1 promoter (Fig. 7).
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