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Published on October 15, 2007

Author: FunSchool

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Chapt. 14 Signal Transduction (also called Cell Signaling) :  Chapt. 14 Signal Transduction (also called Cell Signaling) Fun! Fun! Fun! Like a vacation! Easy and Entertaining! No Headaches! No math! WE COVERED ELECTRICAL SIGNALING (or membrane potential) CONTROLLING CELLS IN CHAPT. 9, NOW WE TALK ABOUT HOW HORMONES WORK!! CHEMICAL MESSENGERS AND THEIR RECEPTORS- INSULIN ACTS THROUGH BINDING ITS RECEPTOR 2 TYPES OF CHEMICAL MEDIATORS::  2 TYPES OF CHEMICAL MEDIATORS: ENDOCRINE PARACRINE ANIMATION:  ANIMATION D:\cell biol 3611\apop cell signaling\ENDOCR LOCAL MEDIATOR A0010401.MOV SIGNAL TRANSDUCTION OVERVIEW:  SIGNAL TRANSDUCTION OVERVIEW 1. CHEMICAL MEDIATORS (CH .14) A. HORMONES – ENDOCRINE- GO THROUGH BLOOD STREAM B. LOCAL MEDIATORS- RELEASED BY ONE CELL, DIFFUSES (CH. 8-9) TO NEXT FEW CELLS LOCATED NEARBY. HISTAMINE, GROWTH FACTORS IN SOME CANCERS 2. CELL TO CELL CONTACT (CH 17) 3. ELECTRICAL (CH. 13) NOBEL LAUREATES (MEDICINE 1985-2003) ALMOST ALL IN SIGNAL TRANSDUCTION:  NOBEL LAUREATES (MEDICINE 1985-2003) ALMOST ALL IN SIGNAL TRANSDUCTION 2003 Paul C. Lauterbur, Sir Peter Mansfield 2002 Sydney Brenner, H. Robert Horvitz, John E. Sulston 2001 Leland H. Hartwell, Tim Hunt, Sir Paul Nurse 2000 Arvid Carlsson, Paul Greengard, Eric R. Kandel 1999 Günter Blobel 1998 Robert F. Furchgott, Louis J. Ignarro, Ferid Murad 1997 Stanley B. Prusiner 1996 Peter C. Doherty, Rolf M. Zinkernagel 1995 Edward B. Lewis, Christiane Nüsslein-Volhard, Eric F. Wieschaus 1994 Alfred G. Gilman, Martin Rodbell 1993 Richard J. Roberts, Phillip A. Sharp 1992 Edmond H. Fischer, Edwin G. Krebs 1991 Erwin Neher, Bert Sakmann 1990 Joseph E. Murray, E. Donnall Thomas 1989 J. Michael Bishop, Harold E. Varmus 1988 Sir James W. Black, Gertrude B. Elion, George H. Hitchings 1987 Susumu Tonegawa 1986 Stanley Cohen, Rita Levi-Montalcini 1985 Michael S. Brown, Joseph L. Goldstein Slide6:  INTEGRAL MEMBRANE PROTEIN HORMONE, CHEMICAL MEDIATOR IMPT KEY HERE TURN ON OR OFF CERTAIN GENES WHAT BONDS BETWEEN LIGAND AND RECEPTOR? FALL 2006 EXAM 1 AVER: 66. FIND EXAM- NAMES ENDING IN your left:A-K MIDDLE: L-S your rt: T-Z:  FALL 2006 EXAM 1 AVER: 66. FIND EXAM- NAMES ENDING IN your left:A-K MIDDLE: L-S your rt: T-Z You can drop an exam; remember to add in extra credit homework SAMPLE GRADE CALCULATION: SCANTRON PORTION: 65 POSSIBLE POINTS, 29 QUESTIONS WORTH 2.24 POINTS EACH NUMBER CORRECT ON SCANTRON TO RIGHT; IF SCORE IS 20, THEN 20 X 2.24 = 44.8, ROUND UP TO 45 PTS. THEN ADD IN THE POINTS IN THE WRITTEN SECTION TOTAL POSSIBLE: 100 PTS General plan for Signal Transduction:  General plan for Signal Transduction Transduction: to carry the signal across the plasma membrane Hormone binds receptor, cascade of events often leads to turning on a transcription factor Transcription factors bind DNA to turn on (or off) certain genes New proteins made to change the cell D:\cell biol 3611\apop cell signaling\cellsig-general.mov RECEPTORS:  RECEPTORS INTEGRAL MEMBRANE PROTEINS TO THRU MEMBRANE WITH ALPHA HELIX HUGE -AVERAGE PROTEIN IN DALTONS: VS. RECEPTOR AT 400,000 DALTONS VERY HIGH AFFINITY FOR HORMONE- WHY? HORMONE BINDS THRU WEAK BONDS, DISTORTS RECEPTOR TO TURN IT ON RECEPTOR CAUSES SECOND MESSENGERS TO BE MADE AND RELEASED INTO CYTOPLASM RECEPTOR DOWNREGUATION:  RECEPTOR DOWNREGUATION RECEPTOR STILL BOUND BY HORMONE, BUT RECEPTOR TURNS OFF BECAUSE REMOVE RECEPTOR FROM PLASMA MEMBRANE BY RECEPTOR-MEDIATED ENDOCYTOSIS (CH. 12) A KINASE (CH. 6) PUTS A PHOSPHATE (OR PHOSPHORYL) FUNC GRP ON RECEPTOR TO TURN OFF RECEPTOR SOME 70% OF MEDICINES WORK ON RECEPTORS::  SOME 70% OF MEDICINES WORK ON RECEPTORS: TOLERANCE: NEOSYNEPHRINE NASAL SPRAY STOPS WORKING AFTER A WHILE DUE TO RECEPTOR DOWN REGULATION ISOPROTERENOL STIMULATES BETA EPINEPHRINE RECEPTOR (STIMULATING HEART) PROPRANOLOL INHIBITS BETA EPINEPHRINE RECEPTOR (REDUCES HEART BEAT) 3 FAMILES OF RECEPTORS IN THE PLASMA MEMBRANE:  3 FAMILES OF RECEPTORS IN THE PLASMA MEMBRANE 1. Ligand gated Channel (see ch. 13) RECEPTOR LINKED TO ION CHANNEL E.G., ACETYLCHOLINE RECEPTOR (SEE OUR WEB SITE ANIMATION; CH. 8/9) THIS CAN BE A VOLTAGE gated ION CHANNEL OR A LIGAND GATED ION CHANNEL. Use the Nerst equation to calc the Vm before and after Ach added. 2. G PROTEIN LINKED RECEPTOR 3. RECEPTOR LINKED TO KINASE 2. G PROTEIN LINKED RECEPTOR:  2. G PROTEIN LINKED RECEPTOR D:\cell biol 3611\apop cell signaling\cellsig-gprotein.mov HORMONE BINDS RECEPTOR, RECEPTOR TURNS ON G PROTEIN, G PROTEIN TURNS ON OTHER PROTEINS G PROTEINS BIND GTP Very large no of Receptors that turn on G proteins –they span the membrane 7 times:  Very large no of Receptors that turn on G proteins –they span the membrane 7 times Figure from “The magnificent seven” science article Slide15:  FIG. 14-5 ANIMATION OF G PROTEIN ACTIVATION:  ANIMATION OF G PROTEIN ACTIVATION 2 on our course web site: http://dkc.mse.jhu.edu/~teal/gprotein.html Another G protein animation: D:\cell biol 3611\apop cell signaling\G PROT ARRESTIN MBC 15_5.mov (sound) Slide17:  GTP ATP P – P – P - P – P – P - SUGAR SUGAR N BASE A N BASE G ENERGY SOURCE AND REGULATOR FOR MICROFILAMENTS (IF ONE PHOSPHATE, MAKES UP DNA ALSO) REGULATOR (IF ONE PHOSPHATE, MAKES UP DNA ALSO) cAMP SUGAR N BASE A P C = CYCLIC; A Second Messenger; REGULATOR Slide18:  FIG. 14-7 FIRST SYSTEM cAMP system (note it uses a G protein) Slide19:  This G protein is called Gs because it stimualtes adenylyl cyclase (Gi inhibits) STIMULATES PROTEIN KINASE A PROTEIN KINASE A ACTIVATED BY 2 cAMP molecules fig. 14-8:  PROTEIN KINASE A ACTIVATED BY 2 cAMP molecules fig. 14-8 G protein activates Adenylyl Cyclase, Protein kinase A, and then a transcription factor:  G protein activates Adenylyl Cyclase, Protein kinase A, and then a transcription factor D:\cell biol 3611\apop cell signaling\MBC cAMP 15_4.mov From our text (a bit too simple) D:\cell biol 3611\apop cell signaling\camp.mov D:\cell biol 3611\apop cell signaling\epi cAMP.mov :  From our text (a bit too simple) D:\cell biol 3611\apop cell signaling\camp.mov D:\cell biol 3611\apop cell signaling\epi cAMP.mov HOW EPINEPHRINE WORKS Summary of how cAMP signal is turned off:  Summary of how cAMP signal is turned off HORMONE LEVELS DECLINE ALPHA SUBUNIT OF G PROTEIN TURNS ITSELF OFF (BREAKS DOWN GTP TO GDP) BETA AND GAMMA SUBUNITS AGAIN BIND TO ALPHA SUBUNIT TO INHIBIT ALPHA cAMP IS BROKEN DOWN BY PHOSPHODIESTERASE THIS PHOSPHODIESTERASE IS TARGET OF MANY MEDICINES THAT RAISE cAMP (e.g, some diuretics) Two G protein Diseases:  Two G protein Diseases 1. CHOLERA BACTERIUM RELEASES A TOXIN THAT ENTERS THE CELL AND PREVENTS Gs FROM BREAKING DOWN GTP TO GDP; THUS GS ALWAYS ON THIS MEANS THAT ADENYLYL CYCLASE IS ALWAYS STIMULATED...SO TOO MUCH cAMP IS MADE DIARRHEA  DEATH THRU DEHYDRATION 2. PERTUSSIS TOXIN; INHIBITS Gi SO CAN’T SHUT OFF ADENYLYL CYCLASE CAUSES WHOOPING COUGH SECOND SYSTEM: InsP3 (OR IP3) SYSTEM (I simplified fig. 14-9):  SECOND SYSTEM: InsP3 (OR IP3) SYSTEM (I simplified fig. 14-9) IP3 released by ACETYLCHOLINE PIP2: 2 fatty acids, Glycerol backbone, Phosphate and Charged molecule (inositol with P) P FACE OF MEMBRANE P inositol SUGAR P P PHOSPHOLIPASE C THIS FRAGMENT IS IP3 WHICH THEN CAUSES RELEASE OF CALCIUM INSIDE CELL THIS PHOSPHOLIPID IS PIP2 (sugar with 2 extra phosphates) Slide26:  SECOND SIGNAL TRANSDUCTION SYSTEM- THE InsP3 OR IP3 SYSTEM THIS IS PHOSPHOLIPASE C BETA FORM AND Gq (NOT Gs OR Gi) Slide27:  BOOK ERROR: ACTIVE DAG IS WHAT IS LEFT IN MEMBRANE: (NOT cAMP-dept PROTEIN KINASE A) ANIMATION OF IP3 SYSTEM:  ANIMATION OF IP3 SYSTEM D:\cell biol 3611\apop cell signaling\PI turnover mcbio.mov (IGNORE “SOC) 2 TYPES OF PHOSPHOLIPASE C: :  2 TYPES OF PHOSPHOLIPASE C: PLC BETA; ACTIVATED BY G PROTEINS CALLED Gq (THIRD TYPE OF G PROTEIN) PLC GAMMA; ACTIVATED BY TYROSINE KINASE (A KINASE THAT PUTS PHOSPHATE ON TYROSINE TYROSINE IS SAME AMINO ACID THAT WE DISCUSSED IN CARBOXYPEPTIDASE A MECHANISM PHOSPHOLIPASE C –GAMMA ACTIVATION BY TYR KINASE::  PHOSPHOLIPASE C –GAMMA ACTIVATION BY TYR KINASE: Summary: PLC gamma activation through tyrosine kinase and beta activation through G protein:  Summary: PLC gamma activation through tyrosine kinase and beta activation through G protein D:\cell biol 3611\apop cell signaling\rectyr.mov D:\cell biol 3611\apop cell signaling\plc becker.mov Second type of PLC, PHOSPHOLIPASE C GAMMA, ACTIVATED BY TYR. KINASE; DISCUSSED LATER IN TEXT:  Second type of PLC, PHOSPHOLIPASE C GAMMA, ACTIVATED BY TYR. KINASE; DISCUSSED LATER IN TEXT WHAT DOES RELEASE OF CALCIUM INTO CYTOPLASM CAUSE? CALCIUM BINDS AND ACTIVATES CALMODULIN Slide33:  WHEN Ca BINDS THIS BENDS 90o WHY? First example of IP3 system: CALCIUM RELEASE AT FERTILIZATION (PLC-GAMMA) (see FIG. 14-14):  First example of IP3 system: CALCIUM RELEASE AT FERTILIZATION (PLC-GAMMA) (see FIG. 14-14) Sperm bind and turn on a tyrosine kinase, stimulate PLC gamma, increasing IP3, and then calcium increases– and a wave of elevated calcium travels across the egg This begins fertilization D:\cell biol 3611\apop cell signaling\ca wave fert.mov 2nd example of IP3; EPINEPHRINE STIM. BOTH cAMP and IP3 PATHS :  2nd example of IP3; EPINEPHRINE STIM. BOTH cAMP and IP3 PATHS FIG. 14-23 Gq, Gi or Gs?? CALCIUM SIGNALING—SUMMARY AND BIG PICTURE BEFORE IP3 INCREASES, NOTE THAT CELLS KEEP CALCIUM VERY VERY LOW IN THE CYTOPLASM-- HOW? TWO MEMBRANE PROTEINS CALLED CALCIUM PUMPS REMOVE CALCIUM ALSO, NOTE THAT CALCIUM CAN INCREASE DUE TO OPENING OF CA CHANNEL IN PLASMA MEMBRANE:  CALCIUM SIGNALING—SUMMARY AND BIG PICTURE BEFORE IP3 INCREASES, NOTE THAT CELLS KEEP CALCIUM VERY VERY LOW IN THE CYTOPLASM-- HOW? TWO MEMBRANE PROTEINS CALLED CALCIUM PUMPS REMOVE CALCIUM ALSO, NOTE THAT CALCIUM CAN INCREASE DUE TO OPENING OF CA CHANNEL IN PLASMA MEMBRANE Slide37:  LIGAND OR VOLTAGE REG. CHANNEL 2 Ca PUMPS PLC BETA OR GAMMA? Summary FIRST 2 SYSTEMS::  Summary FIRST 2 SYSTEMS: 1st SYSTEM: cAMP PATH; HORMONE BINDS SERPENTINE RECEPTOR, TURNS ON G PROTEIN, TURNS ON ADENYLYL CYCLASE, cAMP LEVELS INCREASE, PKA STIMULATED 2ND SYSTEM: IP3 PATH, TWO TYPES: SERPENTINE RECEPTOR TURNS ON G PROTEIN, PHOSPHOLIPASE C BETA, PIP2 BROKEN DOWN TO IP3 (CALCIUM RELEASE) AND DAG (PKC). RECEPTOR IS A TYROSINE KINASE THAT TURNS ON PHOSPHOLIPASE C GAMMA. 3rd SYSTEM: NITRIC OXIDE (NO) CAUSES VASO- DILATION:  3rd SYSTEM: NITRIC OXIDE (NO) CAUSES VASO- DILATION SAME IP3 SYSTEM AS IN FIG. 14-16 NEW ENZYME GUANYLYL CYLASE MAKES cGMP (NOT cAMP) BOND? NO SYSTEM; NOBEL IN 1999:  NO SYSTEM; NOBEL IN 1999 ACETYLCHOLINE EXPANDS BLOOD VESSELS INCLUDING DURING PENILE ERECTION VIGAGRA PREVENTS THE DESTRUCTION OF cGMP VIAGRA INHIBITS cGMP PHOSPHODIESTERASE 4TH SYSTEM: TYROSINE KINASES:  4TH SYSTEM: TYROSINE KINASES WE ALREADY DISCUSSED; HORMONE BINDS RECEPTOR, RECEPTOR IS A TYROSINE KINASE 2 RECEPTORS HAVE TO DIMERIZE THE DIMERIZED RECEPTORS TURN EACH OTHER ON- autophosphorylation RECEPTORS TURN ON PHOSPHOLIPASE C GAMMA EXAMPLES: INSULIN, GROWTH FACTORS 4TH SYSTEM: TYROSINE KINASES:  4TH SYSTEM: TYROSINE KINASES DIMERIZATION AUTOPHOSPHORYLATION INSULIN & GROWTH FACTORS USE THIS TYPE OF RECEPTOR ON RECEPTORS ARE OFF When HER2 (human epidermal growth factor receptor 2) gene is found in multiple copies, extra HER2 protein receptors are produced and this over-expression of HER2 causes 20% to 30% of breast cancer. Herceptin is an antibody that binds to EGF receptor 2 (HER2) and blocks the activation of EGF receptors:  When HER2 (human epidermal growth factor receptor 2) gene is found in multiple copies, extra HER2 protein receptors are produced and this over-expression of HER2 causes 20% to 30% of breast cancer. Herceptin is an antibody that binds to EGF receptor 2 (HER2) and blocks the activation of EGF receptors Help session for Exam 2 2006:  Help session for Exam 2 2006 North Classroom 1533 4-5 pm Oct. 18 Wed (day before exam 2) Today’s lecture material is the last for Exam 2 REMEMBER to use the free tutoring at the Center for Learning Assistance (2 bio tutors…) NOW PROTEINS WITH AN “SH2” DOMAIN CAN BIND TO THE PHOSPHORYLATED TYROSINES:  NOW PROTEINS WITH AN “SH2” DOMAIN CAN BIND TO THE PHOSPHORYLATED TYROSINES SEE ANIMATION PHOSPHOLIPASE C GAMMA SH2 DOMAIN OF PLC GAMMA NOW PLC GAMMA ON 4TH SYSTEM CONT’D: TYROSINE KINASE TURNS ON MAP KINASE PATH:  4TH SYSTEM CONT’D: TYROSINE KINASE TURNS ON MAP KINASE PATH DON’T MEMORIZE STEPS GRB2 HAS SH2 MAP KINASE TURNS ON TRANSCRIPTION FACTORS, TURNS ON GENES RECEPTOR TYROSINE KINASE PATH LINKS TO (1) PLC AND (2)MAP KINASE PATH; SEE ANIMATIONS (note; click on for my my hard drive):  RECEPTOR TYROSINE KINASE PATH LINKS TO (1) PLC AND (2)MAP KINASE PATH; SEE ANIMATIONS (note; click on for my my hard drive) D:\cell biol 3611\apop cell signaling\rectyr.mov D:\cell biol 3611\apop cell signaling\plc becker.mov http://biocreations.com/pages/bioanimations.html then click on animation or… D:\cell biol 3611\apop cell signaling\MAPK1.swf (Biocreations) Review the animations on the class web site. See more info on the receptor tyrosine kinases and cancer/human disease. 4TH PATH CONT’D: (don’t memorize for exam) :  4TH PATH CONT’D: (don’t memorize for exam) ANTHRAX ACTS IN PART BY INACTIVATING MAP KINASE PATH (SCI 280:734, 1998) This web site centers in on the epidermal growth factor (EGF) receptor and drugs that inhibit this receptor TYROSINE kinase will stop cancer.  For example, AstraZeneca has a drug called Iressa, Novartis has Gleevec and Genentech has Herceptin.  Old: http://www.egfr-info.com/ Erbitux (ImClone, Bristol-Myers Squibb Co) is another antibody to EGF receptor and this drug was associated with the stock scandal that caused Martha Stewart jail time! At first, they thought it did not work (stock went downhill); now they think it DOES! POOR MARTHA! Slide49:  52% decrease in the recurrence of breast cancer THE GOOD (BCL-2), :  THE GOOD (BCL-2), THE BAD APOPTOSIS: AND THE UGLY 5TH SYSTEM; APOPTOSIS:  5TH SYSTEM; APOPTOSIS NECROSIS (CELL APOPTOSIS BURSTS; (NO BURSTING INFLAMMATION). OR INFLAMMATION). NORMAL CELL ENGULFS THE APOPTOTIC CELL. (FROM MOL BIO CELL) WHY IS APOPTOSIS IMPORTANT?:  WHY IS APOPTOSIS IMPORTANT? NEEDED FOR DEVELOPMENT OF EMBRYO, SCULPTING OF ORGANS, BODY NOBEL PRIZE ON APOPTOSIS: “MANY (CANCER) TREATMENT STRATEGIES ARE BASED ON STIMULATION OF THE CELLULAR 'SUICIDE PROGRAM.” ~ SO CANCER CELLS WOULD KILL THEMSELVES! EXAMPLES OF APOPTOSIS OR PROGRAMMED CELL SUICIDE::  EXAMPLES OF APOPTOSIS OR PROGRAMMED CELL SUICIDE: If UV light damages a cell’s DNA, then that cell will undergo cell suicide (apoptosis)- if not cancer. EMBRYONIC BRAIN HAS TOO MANY CELLS; MANY DIE BY APOPTOSIS (IF APOPTOSIS IS PREVENTED, RETARDATION RESULTS). Slide54:  NORMAL MICE NO APOPTOSIS IF BLOCK APOPTOSIS== OVERPROLIFERATION OF BRAIN CELLS CAUSES MENTAL PROBLEMS, WEBBED DIGITS OF MOUSE EMBRYO EXAMPLES OF APOPTOSIS OR PROGRAMMED CELL SUICIDE::  EXAMPLES OF APOPTOSIS OR PROGRAMMED CELL SUICIDE: EMBRYOS HAVE WEBBING- THE WEBBING CELLS ARE PROGRAMMED TO UNDERGO APOPTOSIS! Rat embryonic digits (Mol Bio Cell) EXAMPLES OF APOPTOSIS OR PROGRAMMED CELL SUICIDE::  EXAMPLES OF APOPTOSIS OR PROGRAMMED CELL SUICIDE: LOSS OF TADPOLE TAIL APOPTOSIS AND HUMAN HEALTH:  APOPTOSIS AND HUMAN HEALTH EXCESSIVE APOPTOSIS OCCURS IN AIDS, NEUROGENERATIVE DISEASES, STROKE AND MYOCARDIAL INFARCTION. IN OPPOSITION, IN AUTOIMMUNE DISEASE OR CANCER, THERE IS AN INHIBITION OF APOPTOSIS (LEADING TO THE SURVIVAL OF CANCER CELLS) BCL-2 IS CENTRAL TO APOPTOSIS:  BCL-2 IS CENTRAL TO APOPTOSIS ALL CELLS OF THE EMBRYO WOULD DIE EXCEPT THAT BCL-2 IS ACTIVATED IN SOME AND THESE CELLS SURVIVE. SO, MUTATE BCL-2 (KILLING THE GENE), ALL EMBRYONIC CELLS DIE. CAN WE MUTATE BCL-2 IN HUMAN CANCER CELLS, KILLING THE CANCER? OR SAVE DESIRED, DYING CELLS BY TURNING ON BCL-2? FIG. 14-25 APOPTOSIS PROCESS:  FIG. 14-25 APOPTOSIS PROCESS 2 PATHS TO APOPTOSIS:  2 PATHS TO APOPTOSIS FAS INDUCES APOPTOSIS TROPHIC FACTOR NOT PRESENT Slide61:  Same path, different figure: THE FAS PATH TO APOPTOSIS FROM MOLECULAR BIOL OF THE CELL STARTS APOPTOSIS CELL DEATH SIGNAL SIMPLIFY: FAS LIGAND BINDS TO FAS. FAS TURNS ON CASPASE 3 CASPASE 3 EXECUTES THE CELL :  CELL DEATH SIGNAL SIMPLIFY: FAS LIGAND BINDS TO FAS. FAS TURNS ON CASPASE 3 CASPASE 3 EXECUTES THE CELL Slide63:  BAD IS TURNED OFF BY THE TROPHIC FACTOR RECEPTOR BCL-2 PREVENTS APOPTOSIS SECOND PATH TROPHIC FACTOR ABSENT OR DNA DAMAGED- BAD IS ON, INHIBITS BCL-2 2ND PATH TO APOPTOSIS AGAIN :  2ND PATH TO APOPTOSIS AGAIN NO TROPHIC FACTOR OUTSIDE CELL OR DNA DAMAGE BAD IS ON BAD INHIBITS BCL-2 BCL-2 NO LONGER INHIBITS CYT. C LOSS FROM MITO- CHONDRIA Cyt C lost, binds APAF-1 CASPASES APAF-1 STIMULATES APOPTOSIS DNA DAMAGE P53 MITOCHONDRIAL PATH…WITH TROPHIC FACTOR PRESENT :  MITOCHONDRIAL PATH…WITH TROPHIC FACTOR PRESENT TROPHIC FACTOR BINDS RECEPTOR; TELLS CELL NOT TO COMMIT SUICIDE BAD OFF BAD NO LONGER INHIBITS BCL-2 BCL-2 PREVENTS CYTOCHROME C MOVEMENT OUT OF MITOCHONDRIA; APAF, CASPASE NOT STIMULATED NO APOPTOSIS MEMBRANE VIEW APOPTOSIS ANIMATION; SEE COURSE WEB SITE:  VIEW APOPTOSIS ANIMATION; SEE COURSE WEB SITE D:\cell biol 3611\apop cell signaling\apoptosis.mov Slide67:  More fat (or less exercise), less apoptosis in cancer cells, more cancer. Cancer cells know they are supposed to die by apoptosis, but somehow prevent the cell suicide p53 Slide68:  BCL-2 BAD CELL

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