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SET 10
Biochemistry/Lab (CHEM 3650)
Nova Southeastern University
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SET 10
What type of membrane does a cell have? Plasma membrane
What does the plasma membrane look like? Double lipid bilayer
What do lipids in the membrane look like? Phospholipids; polar head with two fatty acid tails (hydrophobic)
Integral protein spans the whole membrane
Peripheral protein attached on only one end of the membrane; can be either external or internal
Three main classes of lipids cholesterol, phospholipids, glycolipids
Cholesterol backbone of steroids ex. testosterone, estrogen, etc
Cholesterol Structure Be able to recognize this!
Types of phospholipids glycerophospholipids and sphingolipids
Structure of glycerophosopholipids backbone is glycerol two fatty acid chains phosphate with an alcohol on the third chain
Structure of sphingolipids (phospholipid) sphingolipid backbone one fatty acid chain phosphate with choline chain
Structure of sphingolipids (glycolipids) sphingolipid backbone one fatty acid chain mono or oligo- saccharide
Glycosphingolipids contain a mono or oligosaccaride (glycolipid)
Gangliosides subset of glycosphingolipids that contain sialic acid (NANA)
Globoside generic name for a glycosphingolipid with more than 3 saccharide units that does not have a specific name
Glycerophospholid (Phosphatidyl Choline) fatty acid; saturated so more solid at room temperature more compact structure; unsaturated and distance gives fluidity
Gated Channels transmembrane protein - pore for ions; transmembrane proteins are used
Voltage-gated gated channel that is stimulated by voltage changes (action potential) across the membrane
Ligand-gated gated channel that is stimulated by ligand binding ex. insulin/acetylcholine binding
Phosphorylation-gated gated channel that is stimulated by phosphorylation on the protein ex. receptor tyrosine kinases
Active Transport requires energy and protein (proximal nephron) transport against the concentration gradient
Coupled Transporters one molecule goes down its concentration gradient while another molecule goes against it
Sodium-Potassium Pump Sodium enters the channel from the cytoplasm and causes a conformational change. This change makes the channel more susceptible for phosphorylation which then causes the channel to change more. This second change opens the pump to the extracellular fluid. Now potassium can bind which causes another conformational change dephosphorylating it and the pump reopens to the cytoplasm releasing the potassium.
Vesicular Transport
2 main types: endocytosis and exocytosis
Endocytosis vesicular transport into the cell
Pinocytosis (type of endocytosis) vesicle around fluid containing molecules; the cell forms a vesicle and engulfs something that was in the extracellular fluid and brings it in; it's non-specific
Phagocytosis (type of endocytosis) brings in a particular material not just fluid
Receptor-mediated endocytosis (type of endocytosis) clathrin-mediated endocytosis internalization of membrane-bound receptors in vesicles
Potocytosis (type of endocytosis) caveolae-mediated endocytosis
Exocytosis vesicular transport out of the cell
Components of the Animal Cell Plasma membrane, cytoplasm, mitochondria, cytoskeleton, nucleus, smooth endoplasmic reticulum, rough endoplasmic reticulum, peroxisome, lysosome, centriole, ribosome
Lyosomes intracellular digestive organelles system of the cell; surrounded by a single membrane acidic environment pH = 5.
-future goal: gene replacement therapy
Tay-Sachs Disease Enzyme: β-Hexoaminidase A Substrate build up: Ganglioside GM
Tay-Sachs Symptoms Mental retardation, blindness, cherry red spot on macula (due to swelling and necrosis of ganglion cells in eye) death: 2-3 years old
Sandhoff-Jatzkewitz Disease Enzyme: β-Hexoaminadase A and B Substrates: Ganglioside GM2 AND globosides (brain and spleen) -Same presentation as Tay-Sachs but more rapidly progressing course -To differentiate you have to see what there is an accumulation of
Generalized Gangliosidosis Enzyme: β-galactosidase Substrate: Ganglioside GM Symptoms: mental retardation, liver enlargement, skeletal involvement
Fabry Disease Enzyme: α-galactosidase A Substrate: ceramide trihexoside Symptoms: skinn rash, kidney failure, pain in lower extremities
Gaucher Disease Enzyme: β-glucocerebrosidase (or β-glucosidase) Substrate: glucocerebroside
Symptoms: liver and spleen enlargement, erosion of long bones and pelvis, mental retardation in infantile form only
Niemann-Pick Disease (No Man picks his nose with his "s"phinger) Enzyme: sphingomyelinase Substrate: Sphingomyelin Symptom: liver and spleen enlargement, mental retardation
Three Types of Cell Signaling Endocrine, Paracrine, Autocrine
Endocrine enter blood directly - travel some distance and exert action on other cells
Paracrine secreted by one cell and exert action on neighboring cells
Autocrine cell secretes chemical which acts on the same cell; it activates its own receptor
Cell Signaling A secretion stimulus that sends a signal to the secretory cell to produce a chemical messenger. The chemical messenger then goes to the receptor which can be intracellular (steroids) or on the surface. By binding the receptor, there is a cascade of changes which will lead to a change in transcription of genes (either upregulation or downregulation
Chemical Messengers (Nervous System) small-molecule neurotransmitters (acetylcholine)
Hypertrophy increased cell size
Intracellular Receptors binds hydrophobic molecules
Result: alter gene expression
Cell-Surface Receptors bind hydrophilic molecules
Result: alter gene expression
Cell Surface Receptors (Ion channel) Ligands - ions; e. Acetylcholine receptors
Cell Surface Receptors (Kinase-related) ligand binds - kinase intracellular domain is activated
Heptahelical Receptors 7-membrane spanning domains; most common type of receptors
Receptor tyrosine kinase causes homo/hetero dimerization and triggers the domain causing phosphorylation; Growth factor binds to the receptor and the receptors dimerize causing a conformational change that activates the tyrosine kinase domain which causes a cross phosphorylation. This phosphorylation causes a signal cascade downstream
JAK-STAT
similar to tyrosine kinase receptor but there is no intrinsic domain of dimerization so another protein (JAK) causes the phosphorylation and triggers the cascade
Serine-threonine kinase receptors conformational changes activates the kinase domain and similar things happen
G-protein coupled receptors Receptor on the surface which is intrinsically bound to a G protein (a protein that binds GTP and GDP); the main function of the protein is to hydrolyze GTP --> GDP. It is active when bound to GTP. When bound to a ligand, G protein will release GDP and bind to GTP (active) which then causes the activation of adenylyl cyclase which cyclizes adenine. It then causes the activation of downstream molecule. If this stays active you get a build up of cAMP. Intrinsic timing turns on the intrinsic activity which cleaves GTP --> GDP turning of the enzyme
Myasthenia Gravis see word document
Cholera see word document
Cancer group of diseases in which cells no longer respond to normal restrains on growth and are resistant to apoptosis precursor: normal cell
Rule of cancer for every oncogene there is a proto-oncogene
oncogene any protein that causes an increase in cell proliferation
see word document
Loss of function Mutations (DNA Repair Enzymes) leads to loss of a gene that keeps the cell under control; it allows for defects in DNA to persist and then causes cancerous cells (like Lynch Disease - HNPCC)
Signal Transduction Cascades Increase in growth factors or receptors causes an overexpression of growth factors or very active receptors which causes a proliferation of cells causing cancer
- also can occur in mutations in signal transduction pathway or mutations in transcription factors
RET proto-oncogene) Receptor Tyrosine Kinase - gain of function causes Multiple Endocrine Neoplasia (MEN) Type 2a and 2b Mutation causes a gain of function because it's active without the ligand bound**
Mutated Zinc Finger Transcription Factor gain of function causes excessive proliferation ex. Wilms Tumor
SET 10
Course: Biochemistry/Lab (CHEM 3650)
University: Nova Southeastern University
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