Lecture 7 - BioE10: Lecture BioE10: Lecture 7 Professor...

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ioE10: Lecture 7 Professor Irina Conboy BioE10: Lecture 7 Engineering desired function into cells Signaling pathways: from plasma membrane to nucleus (and back). Dynamic adaptation to ever-changing environments
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Objectives: In order to develop designer micro- and nano-tools for controlling cell behavior we need to understand how cell behavior is typically controlled by dynamic signaling pathways that interact precisely in space and time to maintain molecular homeostasis in ever-changing environments. Biological fundamentals: Plasma membrane, receptor, ligand Second messenger, phosphoryllation; de-phosphoryllaiton; Kinase, phosphatase Maps of Notch, TGF- , MAPK, STAT/Jak pathways Cyclin; CDK; yclin degradation; proteasome; Cyclin degradation; proteasome; Autophagy, lysosome
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Changing gene expression in response to an outside signal adapting N-terminus (outside) Ligand (receptor binding and activation) C-terminus (inside) Receptor-associated kinase (inside); ould be C rminus of receptor itself Could be C-terminus of receptor itself Lipid bi-layer of plasma membrane Inactive transcriptional factors in cytoplasm Second messengers facilitate association between signaling molecules in a pathway Transcriptional factors activated by kinase and dimerized can travel to nucleus and function there
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Protein phosphorylation (kinase) de-phosphorylation (phosphatase) changes structure and function of proteins, e.g. nuclear translocation; Threonine Serine Tyrosine interactions with other proteins, enzymatic activity, etc. C H H C H C H H 3 N + C00 - H 3 N + C00 - H 3 N + C00 - CH 2 OH CH OH CH 3 CH 2 O Protein +ATP Protein O P O +ADP Kinase Phosphatase O P i H 2 0 p
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IL-6 Stat/Jak pathway: dimerization of transcriptional factors CAS=constitutively active Stat IJK=Inactive Jak kinase Mutant forms of some STAT proteins have been shown to bind DNA in the a e bee s o to b d t e absence of any external signal and to activate unregulated cell growth. Insertion of a cysteine residue that results in constitutive dimerization of STAT3 causes tumor production in mice Q: What mutations/changes of function of the JAK/Stat pathway genes would result in A. cancers; B. stem cell deficiencies? Q: design synthetic circuitry with negative feedback that enables induction of IJK by high Stat activation and CAS by low tat activation. p21 Cell division Stat activation.
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Map kinase (mitogen-activated) Signal Transduction Pathway: Ser-Thr phosphoryllation cascade nuclear translocation/transcriptional activation Q: what are the main functions of negative feed- back loops in this Phosphatases pathway? And in signaling pathways in eneral? general? Or Jun Gene A http://www.bio.davidson.edu/courses/Immunology/Flash/MAPK.html
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http://www.nature.com/nrn/journal/v2/n10/animation/nrn1001-734a_swf_MEDIA1.html NF-kB pathway: de-repression of TF (permission to translocate to nucleus) Abcam
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Wingless (Wnt) signaling pathway: de-repression/stabilization of TF-beta-catenin Promega
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Notch signaling pathway: ligand-induced cleavage of C-terminus of Notch receptor
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This note was uploaded on 04/21/2010 for the course BIOE 10 taught by Professor Conboy during the Fall '09 term at University of California, Berkeley.

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Lecture 7 - BioE10: Lecture BioE10: Lecture 7 Professor...

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