BIOL 3611-001 exam 3 study guide

What are the Six cell signaling pathways?

∙ Six cell signaling pathways

o cAMP  

▪ uses G protein

∙ Gs: stimulates

∙ Gi inhibits

∙ G protein diseases

o Cholera: prevents Gs from breaking down GTP to GDP

▪ Adenylyl cyclase is always on, too much cAMP

▪ cAMP stimulates Cystic Fibrosis Chloride  

Transporter which leads to diarrhea, death due to  

dehydration  

o pertussis toxin: inhibits Gi

▪ adenylyl cyclase stays on

▪ too much cAMP in the lungs, whooping cough

▪ ATP  

∙ Sugar  

∙ Nitrogenous base

▪ Adenylyl cyclase comes in

▪ Cyclic AMP formed

∙ Stimulates protein kinase A  

▪ Phosphodiesterase lowers cAMP

∙ High phosphodiesterase causes lower epinephrine

▪ It’s a second messenger and a regulator  

o ion channel

▪ acetylcholine nicotinic receptor

What is ATP?

∙ an Na channel

∙ no G proteins  

∙ Ach binds to alpha subunits in the receptor to open If you want to learn more check out what is the principle task in management?

∙ Na goes into the cell

▪ acetylcholine muscarinic receptor

∙ Gq protein

∙ Opens a K channel

∙ Ligand gated

o Ach binds to receptor

o Gq is activated

o Beta gamma subunits bind to ion channel

o K channel opens, K goes out of the cell

o IP3-Ca release

▪ Epinephrine alpha receptors

▪ Ach releases IP3

▪ Gq protein

▪ PIP2: 2 fatty acids, glycerol backbone, phosphate and charged molecule ▪ Phospholipase C cuts bond between the phosphate and the glucose ∙ Leaves a sugar with two extra phosphates (IP3)

▪ IP3 causes the release of calcium from the endoplasm reticular ▪ DAG is left over

∙ Activates protein kinase C We also discuss several other topics like what is Dyadic Communication?

▪ Calcium release into the cytoplasm binds to and activates calmodulin ∙ Ca-calmodulin complex then binds and activated other proteins ∙ Causes alpha helix bends so the complex can wrap around blood  vessels

What is IP3-Ca release?

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o Causes vasoconstriction during fight or flight situations

▪ Calcium pumps

∙ In the plasma membrane

∙ In the ER membrane

∙ Keep Ca low in the cell

o NO (nitric oxide)

▪ Ach muscarinic receptors and g proteins introduce IP3s to the cell ▪ Calcium is released

▪ Calmodulin gets activated

▪ NO synthase gets activated

▪ NO is made

▪ NO activates guanylyl cyclase

▪ cGMP is made which activates protein kinase G

▪ Leads to the relaxation of blood vessels

o Tyrosine kinase receptors

▪ Hormone binds to the tyrosine kinase receptor

▪ A phosphate is added to tyrosine (an amino acid)

▪ Two receptors dimerize to turn each other on

∙ They phosphorylate each other

▪ The activated receptors turn on Map kinase, PLC and PI3 kinase ▪ Examples: insulin and growth factors

∙ Map kinase pathway:

o RAS (a G protein)

o MAPK

o Kinase cascade

o Transcription factors turned on

o Genes for cell division are turned on If you want to learn more check out What did the Native Americans do with Christianity?

∙ Growth factor (and insulin) receptor:

o Stimulates PLC  

o Releases calcium

∙ Growth factor receptor:

o Stimulates PI3 kinase (Akt)

o Leads to cell survival (prevents apoptosis) and cell division

▪ Cancer:

∙ Hyperactive PI3 kinase pathway

∙ Overactive GF receptor

∙ Too many GR receptors

o Ex. Breast cancer: too many human epidermal growth  If you want to learn more check out When did we became fully human?

factor receptor 2 genes, too many receptors

o Herceptine is an antibody

∙ Mutated RA, RAF, or MEK  

o Steroid

▪ Four connected rings of carbon

∙ Very hydrophobic

▪ Go from bloodstream carrier proteins to plasma membranes  

▪ Plasma membranes to cytoplasmic soluble receptor protein (GR) ▪ GR is the transcription factor

▪ New mRNA is made

▪ New proteins are made

∙ Cell parts

o Nucleus

▪ Nuclear pores: used by proteins (such as transcription factors) to enter the  nucleus and for mRNA to leave the nucleus

▪ Nuclear lamina: within the nuclear envelope

▪ Nuclear envelope: has two membranes, where proteins are made on bound  ribosomes, connects to the rough ER

o Smooth ER

▪ Functions

∙ SER enzymes remove negative phosphate groups from glucose-6-

phosphate

o So glucose can pass through the membrane by facilitated  

diffusion

▪ Glucose -6-phosphate deficiency

∙ Growth retardation

∙ Enlarged kidney and liver

∙ Low blood sugar

∙ Tendency to bleed  

∙ Lowered white blood cells

∙ Infections

∙ Synthesis of many lipids, fatty acids, phospholipids, steroids

∙ Stores calcium

o IP3 receptor located here

∙ Drug breakdown

o Hydroxylation reaction

▪ Hydrophobic drug sticks in the membrane  

∙ NADPH, H, and O are all present

▪ Mixed function oxidases react

▪ Left with hydrophilic compound that is easy to  

urinate out

∙ And NADP, water

▪ Problems:

∙ SER and mixed function oxidases are  

inducible

o Drug addicts have many more than  

clean people

∙ Creates carcinogens

∙ Grapefruit juice inhibits mixed function  

oxidases

o Some medicines become 15 times  

stronger

▪ Overdose

o Rough ER

▪ Receptors for ribosomes

▪ Closer to the nucleus

▪ Continuous, nuclear envelope to RER to SER

▪ Functions

∙ Lipid synthesis

∙ Synthesis of proteins that will be secreted, put into the membrane  or sent to the lysosome

o Ribosomes

▪ Free ribosomes

∙ Not bound to RER

∙ Make proteins that stay in the cytoplasm

▪ Bound ribosomes

∙ Bind to RER

∙ Make plasma membrane proteins, lysosomal proteins, ad secreted  proteins

o Golgi

▪ Cis  

∙ Same side as RER

▪ Trans

∙ Opposite side of RER

▪ Functions

∙ Store sugars

∙ Add and remove sugars from proteins

∙ Moves enzymes to the lysosome

o Enzymes within the lysosome are called acid hydrolases

▪ Acidic to breakdown

▪ Made in the RER

▪ Mannose (sugar) gets phosphorylated

▪ Mannose-6-phosphate binds to receptor

▪ Enzymes are packaged into transport vesicles

▪ Transport enzymes to late endosome

▪ Turns into lysosome

o Lysosomes

▪ Acid hydrolases break down biomolecules to monomers

▪ pH is 4

▪ functions

∙ phagocytosis

∙ receptor mediated endocytosis  

∙ autophagy

o destroys old organelles

∙ exocytosis of lysosome

∙ autolysis  

o death of the entire cell

▪ formation

∙ endosome forms at the plasma membrane

∙ moves to early endosome

∙ acid hydrolases carried to the late endosome

∙ hydrogen is pumped into the lumen of the late endosome

∙ more acidic and mature

∙ lysosome

o peroxisomes

▪ mixed function oxidases

▪ catalase

∙ reacts with hydrogen peroxide to make oxygen and water

▪ function

∙ control oxygen levels in the cell

∙ breakdown of very long chain fatty acids (VLCFA)

o VLCFA anything longer than 16 carbons  

o Broken down in the mitochondria to make ATP

∙ Remove 2 H atoms to break down ethanol, formaldehyde, nitrogen  compounds

o Acetaldehyde produced

o Hydrogen peroxide produced

▪ ALD sink model

▪ Lorenzo’s Oil

∙ Lowers levels of dangerous saturated VLCFA

∙ Competitive inhibition

∙ Exocytosis  

o Starts at RER

▪ Sugars added to nitrogen on the protein

o Golgi

▪ Sugars added to hydroxyl on the protein

o Secretory vesicle

∙ Endocytosis

o Phagocytosis

▪ Ingestion of large particles

▪ Vacuoles fuse with early and late endosomes

▪ Become lysosomes

o Receptor mediated  

▪ Receptor resent

▪ Ligand binds

▪ Receptor ligand complexes diffuse laterally through the membrane ▪ Clathrin coat forms

▪ Invagination

∙ Clathrate binding

▪ Coated endocytic vesicle formation

▪ Uncoating

∙ Adaptor protein recycled

∙ Clathrin recycled

∙ Dynamin recycled

▪ Fusion with early endosome

∙ Release of the ligand

▪ Transport to late endosome

▪ To lysosome  

∙ Breakdown

∙ Snare hypothesis

o Transport vesicle binds 2 tethering proteins  

o t and V snares bind loosely (weak bonding)

o more weak bonds form to wrap snares around each other o strength of the bonds force the membranes together

∙ Secretion pathway

o Nuclear envelope

▪ Proteins made

o Rough ER

▪ Proteins made

▪ Proteins stuck in the lumen of the RER

o Transport vesicles

o Golgi

▪ Adds sugars to the protein

o Secretory vesicles

o Plasma membrane

o Exocytosis