Cystic fibrosis channels. The R-domain has more than one function. In addition to it's inhibitory role in Cystic fibrosis is a hereditary disease that channel gating (when unphosphorylated)the causes certain glands to produce abnormal

Neurodegenerative diseases and ubiquitin-proteasome syster to copyright considerations See Figure chanover, A and Brundin, P. 2003. The ubiquitin proteasome enerative diseases: sometimes the chicken, sometimes the egg

PROTACS: CHIMERIC MOLECULES TO TARGET PROTEINS FOR UBIQUITINATION AND (taken from KM Sakamoto, Mol. Genetics and Metabolism 77(2002)44-56) target targettargettarget target target target target target To circumvent the problem of transducing cells at

Reversible ligation of Ubiquitin and Ubls to other proteins. Figure by MIT OCW. After Figure 1 in Hochstrasser M. Evolution and function of ubiquitin-like protein-conjugation systems. Nat Cell Biol. 2000 Aug:

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How p53 and Rb pathway function may be disrupted in cancer cells Components of the pathway which are found altered in human cancers are shown in red on the diagram above p53 and Rb themselves may be inactivated by gene mutation (loss of both copies or also as in familial retinoblastoma and Li-Fraumeni syndrome where there are inherited mutations in one copy of Rb or p53 gene respectively. Alternatively

Figure 2 in Muratani M, Tansey WP. \How the ubiquitin-proteasome system controls transcription.\ Nat Rev Mol Cell Biol. 2003 Mar; 4(3): 192-201. Regulation of TCR by ubiquitylation of RNA polymerase II. Transcription-coupled repair (TCR)is the mechanism through which mutations in actively transcribed genes are preferentially repaired. a Elongating RNA polymerase II (pol II)

Images removed due to copyright considerations See Fig. 2 in David J. Katzmann, Greg Odorizzi Scott D. Emr RECEPTOR DOWNREGULATION AND MULTIVESICULAR-BODY SORTING Nature Reviews Molecular Cell Biology 3, 893-905(2002); doi: 10.1038/nrm973 See Fig. 7 in: Katzmann DJ, Stefan CJ, Babst M, Emr SD

insolubility. Administration of cystamine, a transglutaminase inhibitor, reduces the To date, 10 neurological diseases, including aggregate formation, retarding the Huntington's and several ataxias, are caused development of neurological phenotype and by the lengthening of glutamine(@) tracts in prolonging the life span of brain cells in various proteins with no obvious functional or transgenic mouse models

Images removed due to copyright considerations. See the following: Figure 1 and Table 1 in Reed SI. 2003. Ratchets and clocks: The cell cycle nover ubiquitylation and protein turnover. Nat Rev. Mol. Cell Biol. 4: 855-864. Figure 1 in Bartek J, Lukas J. Mammalian G1-and S-phase checkpoints in response to DNA damage. Curr Opin Cell