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The C-terminal Src kinase (Csk) phosphorylates and downregulates Src family tyrosine kinases Cell transformation by src oncoproteins is caused by several oncogenic mechanisms, which interfere with this phosphorylation. The CSK gene could therefore potentially function as an antioncogene. The Csk-binding protein (Cbp) localizes Csk close to its substrates at the plasma membrane, and increasesthe specific activity of the kinase. It has been reported prior to occurrence of neoplastic lesions in the colon carcinogenesis; the tumor suppressor gene CterminalSrc kinase (Csk) was down-regulated with a concomitant increase in Src activity. Furthermore, pharmacological or genetic (RNA interference) inhibition of Csk resultedin increased proliferation in colon cancer cell lines through the mitogen-activated protein kinase dependent pathway. Csk, which phosphorylates tyrosine residues in the negative regulatory sites of Src family kinases, downregulated Fyn- and Lck-mediated stimulation of the serum response element and Fynmediated enhancement of IL-2 promoter activity.

DCN1-like protein 2, also known as DCUN1D2, which contains one DCUN1 domain and 1 UBA-like domain, may play a role in the neddylation of cullins that regulate SCF-type ubiquitin ligase complexes. The gene encoding Dcun1D2 exists on human chromosome 13. Chromosome 13 houses key tumor suppressor genes, including BRCA2 and RB1, which are associated with breast cancer susceptibility and retinoblastoma, respectively.