vcyclin

V-cyclin, sometimes written as v-cyclin or vcyclin, is a viral cyclin protein encoded by Kaposi's sarcoma-associated herpesvirus (KSHV). It is a homolog of cellular cyclins, particularly the D-type family, and shares the ability to bind and activate cyclin-dependent kinases (CDKs).

In biochemical studies, v-cyclin forms active kinase complexes with CDKs, notably CDK6 and, in some contexts, CDK2. These complexes can phosphorylate substrates involved in cell-cycle regulation, including members of the retinoblastoma (Rb) protein family, thereby promoting progression from G1 to S phase. Unlike many host cyclins, v-cyclin can drive cell-cycle progression under regulatory conditions that would normally constrain cellular cyclins, and its activity is described as constitutive or abnormally regulated relative to typical cellular cyclins.

Biological significance and disease relevance: v-cyclin is implicated in the manipulation of host cell-cycle control during KSHV infection and is associated with the pathogenesis of KSHV-associated malignancies such as Kaposi's sarcoma and primary effusion lymphoma. The protein has been detected in Kaposi's sarcoma lesions and is considered one factor that may cooperate with other viral proteins to promote proliferation and survival of infected cells. The exact contribution of v-cyclin to oncogenesis is complex and involves interactions with multiple cellular pathways.

Regulation and research: The activity of v-cyclin is a focus of research aimed at understanding viral oncogenesis and how KSHV subverts host cell-cycle checkpoints. Because its CDK partnerships can be less susceptible to certain regulatory controls, v-cyclin presents a potential target for therapeutic strategies against KSHV-related diseases.

Discovery and naming: The term v-cyclin refers to a viral cyclin encoded by KSHV, named for its homology to cellular cyclins. Ongoing studies seek to clarify its precise roles in viral replication and cancer development.