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3-Cell Signaling.pdf

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Department
Biology
Course
Biology 3338A
Professor
Sashko Damjanovski
Semester
Fall

Description
1 •  After fertilization, cytoplasm looks different (D) •  Only at stage (i) transcription starts 2 •  Cell adhesionà cell sticks to each other (CADHERINS) •  Cells like to stick to cells of same type. •  Same cells have greater affinity to each there (will be on inside); less affinity on the outside 3 •  Cadherin is most important cell surface adhesion molecules •  Homophillicà same cadherin on same cell (n-cad are neural etc etc) •  Different cells have different numbers of cadherin and that is how they sort themselves •  A cell expressing e-cad, have a certain number of cadherin they will stick to each other. N-cads have more cadherin,. If put all together, they will sort and form a hierarchy. •  Hierarchy is formed due to different number of cadherin (if had same number would just form a ball) 4 •  Cell cell adhesion is important. Pretty close to cell communication •  Optic cup signals to form lens. Lens induces retina from optic cup. •  Endocrine signalling is important but we won’t really look (not really apparent in embryos) •  Paracrine and juxtacrine •  Paracrine is signalling of very close cells through secreted molecules. Molecule will drift to nearby cells (1 or 2 away). •  Juxtacrine need membranes of cells to touch. Membrane bound interaction. 5 •  Memorize!!! 6 •  Have a cell surface receptor (usually a dimer). Need two receptors are dormant in absent of ligand. In presence of ligand, dimerize and auto activate. Phosphorylate cytoplasmic tail. Become active. Can now phosphorylate other things and activate other proteins. Active proteins can now activate other things. 7 •  A lot of combos of fgf receptors and signalling moleculesà general concept is the same •  fgf 8 is signalling in lens formation 8 •  Cell receptor is one on epidermis •  Need right FGF, ligand and receptor •  When FGF binds, receptor dimerization. Receptor auto phosphorylates and then can activate things •  Series of activation •  ERK is able to get into the nucleus and effect transcription •  All activating cascades •  Activated RAS is potent (need to shut off).; GAPs role is to inactivate RAS •  Activated GEF activates RAS, which is immediately shut off by GAP •  Need more ligands to keep turning it on •  ERK will interact with TF (different transcription factors for every cellà different determinants) 9 •  Same idea: dimerization of receptor as ligands bind •  Autophosphorylates; JAK molecules get phosphorylate causes activation and dimerization of STAT •  STAT goes into nucleus •  ERK inhibits S
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