The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

Links

 

Gene Review

CCDC22  -  coiled-coil domain containing 22

Homo sapiens

Synonyms: CXorf37, Coiled-coil domain-containing protein 22, JM1
 
 
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.
 

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]
 
WikiGenes - Universities