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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Gene Review: 

CCDC22  -  coiled-coil domain containing 22

Homo sapiens

Synonyms: CXorf37, Coiled-coil domain-containing protein 22, JM1
 
 
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Disease relevance of CCDC22

  • The apoptosis related proteins Bax, Bcl-2, and NF-kappaB were analyzed in sanguinarine induced apoptosis and blister cell death (BCD) of K562 erythroleukemia cells and in sanguinarine treated high Bcl-2 expressing JM1 pre-B lymphoblastic cells, utilizing immunofluorescence-flow cytometry [1].
 

High impact information on CCDC22

  • The final band pattern in stimulated lymphocytes resembled that of the malignant T lymphoblastic cell line JM1 [2].
  • The pattern of endogenous substrates which are phosphorylated on tyrosine and threonine residues in the malignant T lymphoblastic cell lines JM1 is likely to be characteristic of proliferating T lymphoid cells rather than of the malignant state, since similar bands appear in normal lymphocytes upon PHA stimulation [2].
  • In contrast, initiation of JM1 cell apoptosis was coincident with dephosphorylation of Bcl-2 and elevated protein phosphatase 2A activity [3].
  • Co-treatment with Z-VAD-fmk (benzyloxy-carbonyl-Val-Ala-Asp-fluoromethylketone), a general caspase inhibitor, significantly prevented cladribine-induced death in JM1 and Jurkat cells for the first approximately 40 h, but not for longer times [4].
  • Cladribine treatment induced mitochondrial transmembrane potential (DeltaPsi(m)) loss, phosphatidylserine exposure, caspase activation and development of typical apoptotic morphology in JM1 (pre-B), Jurkat (T) and U937 (promonocytic) cells [4].
 

Biological context of CCDC22

  • Increased phosphorylation of Bcl-2 protein in the JM1 ALL cell line, achieved by expression of the phosphomimetic Bcl-2 construct S70E, enhanced JM1 cell chemoresistance [3].
  • On the other hand the non-physiological phorbol ester, 12-O-tetradecanoyl phorbol acetate (TPA), a tumour promotor with potency of inducing differentiation in some leukaemic cell lines, induced changes in both normal thymocytes and in the leukaemic line JM1 were inconsistent with maturation, e.g. a fall in the percentage of OKT3 cells [5].
  • Treated JM1 cells, on the other hand, showed an increase in the expression of Bcl-2 protein in both forms of cell death, but failed to show Bax expression [6].
 

Anatomical context of CCDC22

  • Caspase-3 activation was observed in apoptosis of K562 cells but not in BCD or in sanguinarine-treated JM1 cells [6].

References

  1. Bax, Bcl-2, and NF-kappaB expression in sanguinarine induced bimodal cell death. Weerasinghe, P., Hallock, S., Liepins, A. Exp. Mol. Pathol. (2001) [Pubmed]
  2. Phytohemagglutinin-induced changes in tyrosine protein kinase and its endogenous substrates in human lymphocytes. Piga, A., Wickremasinghe, R.G., Taheri, M.R., Yaxley, J.C., Hoffbrand, A.V. Exp. Cell Res. (1985) [Pubmed]
  3. VEGF-induced phosphorylation of Bcl-2 influences B lineage leukemic cell response to apoptotic stimuli. Wang, L., Chen, L., Benincosa, J., Fortney, J., Gibson, L.F. Leukemia (2005) [Pubmed]
  4. Cladribine induces apoptosis in human leukaemia cells by caspase-dependent and -independent pathways acting on mitochondria. Marzo, I., Pérez-Galán, P., Giraldo, P., Rubio-Félix, D., Anel, A., Naval, J. Biochem. J. (2001) [Pubmed]
  5. Biochemical and immunological differentiation of human thymocytes induced by thymic hormones. Ho, A.D., Ma, D.D., Price, G., Hunstein, W., Hoffbrand, A.V. Immunology (1983) [Pubmed]
  6. Role of Bcl-2 family proteins and caspase-3 in sanguinarine-induced bimodal cell death. Weerasinghe, P., Hallock, S., Tang, S.C., Liepins, A. Cell Biol. Toxicol. (2001) [Pubmed]
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