CCNE1

From WikiMD's Wellness Encyclopedia

CCNE1[edit | edit source]

CCNE1 (Cyclin E1) is a protein that in humans is encoded by the CCNE1 gene. Cyclin E1 is a member of the cyclin family, which is characterized by a periodicity in protein abundance through the cell cycle. Cyclins function as regulators of cyclin-dependent kinases (CDKs).

Function[edit | edit source]

Cyclin E1 forms a complex with and functions as a regulatory subunit of CDK2, whose activity is required for cell cycle G1/S transition. The CCNE1 gene is located on chromosome 19q12 and is involved in the regulation of the cell cycle at the G1/S transition. Cyclin E1 accumulates at the G1-S phase boundary and is degraded as cells progress through S phase.

Clinical Significance[edit | edit source]

Overexpression of cyclin E1 has been observed in various types of cancer, including breast, ovarian, and gastric cancers. This overexpression is often associated with poor prognosis and increased tumor aggressiveness. The CCNE1 gene is sometimes amplified in cancer, leading to increased levels of cyclin E1 protein and dysregulation of the cell cycle.

Interactions[edit | edit source]

Cyclin E1 interacts with several proteins, including:

  • CDK2: Cyclin E1 binds to CDK2, forming a complex that is essential for the G1/S transition in the cell cycle.
  • p27^Kip1: This is a cyclin-dependent kinase inhibitor that can bind to the cyclin E1-CDK2 complex, inhibiting its activity.
  • p21^Cip1: Another cyclin-dependent kinase inhibitor that can regulate the activity of the cyclin E1-CDK2 complex.

Research and Therapeutic Implications[edit | edit source]

Given its role in cell cycle regulation and its overexpression in various cancers, cyclin E1 is a potential target for cancer therapy. Inhibitors of the cyclin E1-CDK2 complex are being investigated as potential therapeutic agents. Understanding the regulation of cyclin E1 and its interactions with other cell cycle proteins is crucial for developing targeted cancer therapies.

References[edit | edit source]

External Links[edit | edit source]

Contributors: Prab R. Tumpati, MD