CCND3 (Cyclin D3) is a member of the D-type cyclin family, which includes CCND1 and CCND2. These proteins play critical roles in regulating the cell cycle progression from the G1 to S phase by forming complexes with cyclin-dependent kinases (CDKs), particularly CDK4 and CDK6. The activated kinase complexes phosphorylate retinoblastoma (Rb) proteins, leading to the release of E2F transcription factors and subsequent initiation of DNA synthesis. CCND3 is encoded by the *CCND3* gene located on chromosome 6q21 and is expressed in various tissues, with higher levels observed in lymphoid cells and certain epithelial tissues.
Antibodies targeting CCND3 are essential tools for studying its expression, localization, and function in both physiological and pathological contexts. These antibodies are widely used in techniques such as Western blotting, immunohistochemistry (IHC), immunofluorescence (IF), and flow cytometry to detect CCND3 protein levels in cell lines, tissue samples, or experimental models. Specificity and validation (e.g., knockout cell lines or siRNA-mediated knockdown) are critical to ensure accurate detection, as cross-reactivity with other D-type cyclins can occur.
Dysregulation of CCND3 has been implicated in cancer. While CCND1 is more commonly associated with malignancies (e.g., mantle cell lymphoma via t(11;14) translocation), CCND3 overexpression or genetic alterations are linked to hematopoietic malignancies, including T-cell acute lymphoblastic leukemia (T-ALL) and multiple myeloma. Conversely, reduced CCND3 expression has been observed in some solid tumors. Research using CCND3 antibodies continues to explore its dual role as an oncogene or tumor suppressor, depending on cellular context, and its potential as a therapeutic target.