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27 Cards in this Set
- Front
- Back
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Major organelles and their funtions |
Plasma Membrane - Boundaries and gradients Nucleus - Store and synthesize DNA Lysosome - Digest and break down ER - Rough - Synthesis Proteins - Smooth- detox Golgi - Modify and transport proteins Mitochondria - energy Centrioles - transport Microtublues - Structure and transport Ribosomes - Synthesize Protiens |
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2 types of passive trasport |
Facilitated - "helper" has Vmax Diffusion - Just pass through the cell - Regulated by concentration gradient Channel - Can be voltage gated |
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2 types of active transport |
primary - Pump through with ATP Secondary - Pumping molecules to create a concentration gradient that "Sucks" other molecules along the gradient |
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In Active transport define roles of: - Ion gradients - Co transporters - ATP |
Ion gradients - used in secondary transport to "suck". Can be reason for primary active transport Co-transporters - Can be used in "coupling" when ion gradients are set up ATP - Provides energy to push pull move or set up an ion gradient |
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C&C Endocrine Paracrine Autocrine |
All are signals send to cells Endocrine - to cells far away - INTO THE BLOOD Paracrine - to cells NEARBY Autocrine - to same cell - Most are also Paracrine |
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Intracellular vs Plasma Membrane Receptors How they work and examples |
Intracellular - receptors are inside the cell. Illicit transcription response Eg. Cortisol Plasma membrane - Across the membrane thoght protien modifications Eg. - Serine/Threonine Kinases -Tyrosine Kinases - JAK-Stat Signaling - GPCR |
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Describe roles of cAMP and IP3 |
Secondar messengers |
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List Chain of events following a ligand binding to a Tyrosine Kinase Receptor |
1. Ligand binds 2. the two parts dimerize and auto phosphoralize 3. Phosphate binds to SH2 of GRB Causing change to SH3 4. GRB binds to SOS-Ras 5. GEF - and activated Ras 6. RAS changes from GDP top GTP 7. GTPed RAS binds to RAF and that initiates MAP Kinas pathway OR 1. Binding phosphoalizes and this recruits then Phosphoralizes IRS 3. This recruits PI-3 Kinase that phosphoralizes PI bis to PI tris phospate 4. This binds to PDK-1 and PKB 5. PKD activates PdK-1 and PKN Activated Map cascade |
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Start and stop: Tyrosine Kinase |
Starts when growth factor binds Causes dimerizatio and auto phosphoralization P binds to SD2 Domain of GRB |
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Pathway for generating IP3 |
Phospolipase C (PLC) cleaves IP3 from DAG and IP3 acts as secondary messenger |
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JAK-STAT receptor - Signalling Cascade |
Similar to Tyrosine Kinase but more direct and The Tyrosine Kinase is attached to the receptor 1. Ligand binds to receptor causing dimerization 2. JAK is the Tyrosine Kinase attached to the receptor and it auto phosporalizes 3. This phosphorilated JAK activates the STAT which binds to itself and that GOES STRIGHT TO THE NUCLEUS |
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Serine-Threonine Kinases |
Ligand binds to HETEROdimers 1. Binds to II first and Dimerizes 2. This recruits I and II phosphoralated I 3. I phosphololated R-Smad 4. Once R-Smad is phosphorolated id is relases and binds with Co-Smad R-Smad and Co-Smad migrate to nucleus and illicit transcription response |
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GPCR Signalling Cascade |
Ligand binds 1. This causes A to change from GDP to GTP and dissociate from B&G 2. A and GTP leaves and binds to Adenylyl Cyclase 3. Adenylyl Cyclase converts ATP to cAMP COULD ALSO activate the DAG/IP3 cascade 4. A unit hudrolises GTP top GDP leaved adenylyl Cyclase and the family gets back together |
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Lifespan of cAMP |
1. ATP is converted to cAMP by Adenylyl Cyclase 2. cAMP is then converted back to AMP by cAMP phosphodiesterase |
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6 ways to decrease a Signal |
1. Decreased stimulus 2. Diffusion of messenger 3. Exhausting of receptor DOWNREGULATION 4. Dephosphoraliziation of dimer 5. GTPases 6. Reversal of cAMP and GAD (Phosphodiesterases) |
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role of SH2 in sinalling |
Connect to Pass along signal by connecting to Phosphorilated Tyrosine and Dimerize the attached protein |
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Role of Plekstrin (PK) homology Domains |
Activate other PK domains Take message from exterior to nucleus |
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Coritisol - Domains of binding of receptors - Method of travel through body - Process after intitiaion - How it is terminated |
3 domains of receptor: Transaction, DNA binding, Ligand binding
Travels on Albumen then passes into cell because it is hydrophobic Process: 1. Ligand binding causes Dimerization that exposes nuclear translocation signal. 2. Exposed Nuclear translocation signal allows receptor to pass into nucleus 3. Binds to the GRE that causes expression or suppression of Genes Terminated by decreased cortisol levels caused by cortisol being destroyed in the liver |
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2 fates of inositol triphophate as a messenger (PI) |
1. Phosphoralated and binds to PK-1 and PKD (membrane docking sites) 2. Converted to PIP2 then cleaved by Phospholipase 3 then DG and IP3 acts as secondary messengers |
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How PI can send signal through PDK and PKB |
PI3 Kinase adds another phosphate this provides docking site for Pleskstrin Homology Domains (eg. PDK and PKB) |
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Protiens in RER vs ribosomes |
RER sends to lysosomes, external of cell and membrane
Free ribosomes are for the cytoplasm, mitochindria and peroxisomes |
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Smooth er funtion |
Synthesize phospholipids and TAGs. Detoxify |
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Example of Threonine Serine Receptor |
TGF - Beta |
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Na and K directon in NA-K ATPase |
Na out K in |
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JAK -STAT receptor example |
Epo |
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Termination of JAK STAT |
Not Phosphodiesterases Either SOCS (Suppressor of Cytocine Signaling) OR PIAS (Protein Inhibitors of Activated STAT) |
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GPCR termination and dissociation with GTP and GDP |
When activated GDP and GTP are EXCHANGED To Deactivate, GTP is HYDROLIZED to GDP |
