Why signalling? Multicellular communication Nematodes (C. Elegans) Fruit Flies (Drosophila) to Man Types of cellular communication A B Direct Cell-Cell Gap Junctions Ca 2+ , cAMP A B Juxacrine Cell-Cell interaction via receptors TCR: MHC NCAM:NCAM Kit:Steel (Neural crest formation) Coordinated behaviour to benefit whole organism Autocrine Massive amplification of signal IL-2 and T-cell activation
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Why signalling? Multicellular communication Nematodes (C. Elegans) Fruit Flies (Drosophila) to Man Types of cellular communication A B Direct Cell-Cell.
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Why signalling?Multicellular communication
Nematodes (C. Elegans)Fruit Flies (Drosophila) to Man
Dominant posttranslational protein modification Serine / Threonine (99%); Tyrosine (<1%) Protein Kinases vs Phosphatases Protein Tyrosine Kinases(PTKs):
Receptor PTKs - transmembrane prot. - insulin R - EGFR,PDGFR,FGFR,NGFR
Non-receptor PTKs - intracellular proteins
- c-Src, JAKs,Fak etc.
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The receptor protein-tyrosine kinase families
Hunter et al. 1997
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Switch activated proteins OFF by dephosphorylation
Mitosis ERKPNucleus
X
Mainly work by regulating gene transcription
Signalling via “Cytokine Receptors”
Class I (e.g.IL2R,4R,7R; GHR, PRLR, EPOR ) Class II ( e.g.IFN; IL10R ) No intrinsic enzyme activity Some cytokines may signal via MAPK / PI3K Class I/II signals through: JAK / STAT-
pathway*
*JAK = “just another kinase”/ Janus kinases
STAT= signal transducers and activators of transcription
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PTPs e.g.SHP-1 dephosphorylate activated JAKs or receptors
Other PTPs dephosphorylate STATs
Suppressor of cytokine signalling proteins (SOCS) bind JAKs,compete with STATS for receptor docking, and target bound signalling components for proteasomal degradation
Protein inhibitor of activated STATS (PIAS) inhibit transcriptional activity of STATs