CCND2 — Cyclin D2
CCND2 belongs to a gene co-expression module in 5 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.
CCND2's module in each cell type
| Cell type | Module | Shares the module with | |
|---|---|---|---|
| CD8⁺ T cells | Cytotoxic Gut Effector cytotoxicity | ATP8B4, CD63, CEBPB, CSF1, CTSA, GNLY, GNPTAB, GZMA +3 more | View in SCUBA |
| Enterocytes | Transit-amplifying progenitor Epithelial development | CLINT1, EHF, ELOVL6, HSD17B12, MSI2, PKP2, RBM3, SLC38A1 | View in SCUBA |
| Goblet cells | BMP Signaling Response Epithelial development | CAMK2N1, EIF4A2, GSTA1, GSTA4, ID2, ID3, PDK4, ZBTB10 | View in SCUBA |
| Innate lymphoid cells | Cell Cycle Entry Cell cycle | EIF1B, ENY2, KMT2E, LUZP1, RAB8A, TPM4 | View in SCUBA |
| Mucosal-associated invariant T cell | Chromatin Complex Regulation DNA/chromatin regulation | APEH, CAPZB, CFH, CHTF8, ESYT1, GDI2, HACD4, HCLS1 +9 more |
About the gene
| Chromosome | 12: 4269771-4305353 |
|---|---|
| Predicted location | Intracellular |
| Essential gene | No |
| Protein class | Cancer-related genes, Disease related genes, Human disease related genes, Predicted intracellular proteins |
| Molecular function | Cyclin |
| Biological process | Cell cycle, Cell division |
Function
Regulatory component of the cyclin D2-CDK4 (DC) complex that phosphorylates and inhibits members of the retinoblastoma (RB) protein family including RB1 and regulates the cell-cycle during G(1)/S transition. Phosphorylation of RB1 allows dissociation of the transcription factor E2F from the RB/E2F complex and the subsequent transcription of E2F target genes which are responsible for the progression through the G(1) phase. Hypophosphorylates RB1 in early G(1) phase. Cyclin D-CDK4 complexes are major integrators of various mitogenenic and antimitogenic signals.
Human Protein Atlas · Open Targets · UniProt
Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.