Cell Biology Final Exam
What is the stucture of a G-protein-coupled receptor
- 7 transmembrane domains - extracellular region binds to the extracellular signaling molecule - intracellular region that activates the g-protein to relay the signal
Anti-IAPs and Apoptosis
- Anti-IAPs bind to IAPs and block them - therefore caspases can be active
Sister Chromatic Separation
- Cdc20 activates APC/C - APC promotes the ubiquitylation and degradation of securin - activation of separase breaks down cohesin molecules so the sister chromatids will be able to separate
Proteolysis and the Metaphase to Anaphase Transition
- Cdc20 binds and activates APC/C - Active APC/C or E3 promotes the ubiquitination of M-cyclin - degradation of M-cyclin in proteasome - APC/C complex also degrades S-cyclin and Securin
Pathway starting with G1- Cdk and ending with S-CDK
- G1-Cdk phosphorylates/ninactivates Rb - E2F proteins become active - E2F proteins promote transcription of G1/S and S-cyclins for progression into S phase
Hedgehog signaling when hedgehog molecule is not present (HH)
- HH does not bind to receptor, patched (PTCH - PTCH is unable to inhibit smoothened (smo) - assembly of molecules inside the cytosol that lead to the phosphorylation and cleavage of GLI into GLIr - GLIr migrates into the nucleus, binds to DNA and inhibits the transcription of target genes
Insulin signaling pathway
- Insulin (extracellular signaling receptor) binds to insulin receptor - receptor cross-phosphorylation on tyrosine domains - Insulin Receptor Substrate 1 attaches to the receptor and is phosphorylated - Phosphoinositide 3-kinase docks on the phosphate of IRS-1 and is activated - Phosphoinositide 3-kinase produces PIP3 - PIP3 binds and activates PDK1 - PDK1 phosphorylates and activates Protein Kinase B - PKB phosphorylate/inactivate GSK3 and cannot convert GS to inactive form - (when PKB is inactive, GSK3 is active, and glycogen synthase is inactive)
Why was notch signaling named this?
- Mutation in notch pathway, there is a notched wing in fruit flies
Control of DNA Replication
- ORC is bound to Cdc6 on origin of replication - Helicases bind and Cdc6 leaves complex - S-Cdk phosphorylates the origin recognition complex which recruits the other molecules we need for DNA replication
Ras Activates MAPK Signaling
- Ras binds and activates (MAP kinase kinase kinase) - MAP 3 kinase phosphorylates and activates MAP 2 kinase - MAP 2 kinase phosphorylates and activates MAP kinase - MAP Kinase phosphorylate proteins and change protein activity as well as phosphorylate transcription regulators that promote changes in gene expression
Regulation of the Cyclin-Cdk Complex by Phosphorylation and Dephosphorylation
- Wee1 kinase adds an inhibitory phosphate to Cdk keeping it in the inactive state - Cdc25 phosphatase removes the inhibitory phosphate and returns CDK-cyclin complex to active state
Regulation of Signaling by Proteolysis: Wnt/beta-catenin Signaling with Wnt
- Wnt attaches to and activates its receptor frizzled and its co-receptor LRP - activation stimulates the activation of a molecule called disheveled - disheveled promotes the disassembly of the complex - beta-catenin becomes stable and moves to nucleus, binds to DNA and its cofactors, Left TCF and Groucho - promotes the transcription of Wnt target genes.
Pro-Apoptotic Proteins
- activated BH3 only proteins inhibit anti-apoptotic Bcl2 proteins - Active BAx/Bak are assembled and can release cytochrome c
Steps of the Activation of G Protein
- activated GPCR functions like GEF to drive exchange of GTP for GDP - activation results in conformational changes that allow interaction of alpha subunit and beta-gamma complex with targets - Hydrolysis of GTP by alpha subunit returns G-protein to inactive state (helped by GAP)
Desensitization in GPCR
- activated GPCR stimulates GRK to phosphorylate GPCR on multiple sites - Arrestin binds to phosphorylated GPCR preventing the receptor from interacting and activating g-protein
Intrinsic Pathway of Apoptosis
- activated by a signal from inside the target cell - Apotosis stimulus allows for the release of cytochrome c - cytochrome c activates Apaf1 - Apoptosis protease activating factor 1 (Apaf-1) - apoptosome assembles - apoptosome binds to initiator caspaces which cleave and activate each other - executioner caspases are activated leading to apoptosis
Extrinsic Pathway of Apoptosis
- activated by a signal from outside the target cell - killer lymphocyte that expresses a Fas ligand and binds to the Fas death receptor on the target cell - triggers assembly of FADD adaptor proteins - adaptor proteins allow for the assembly of initiator caspases - adaptor proteins and initiator caspase complex is known as the death inducing signaling complex (DISC) - initiator caspase is activated and promotes activation of the executioner caspase which will trigger apoptosis
Receptor Tyrosine Kinases (RTKs)
- activated by a signal molecule in the form of a dimer - kinases cross-phosphorylate themselves adding phosphate groups to the intracellular domain of the kinases - other intracellular signaling pathways bind to the phosphates and become activated
How are G protein-coupled receptors (GPCRs) activated?
- activated by extracellular signaling molecules (taste and smell. neurotransmitters, hormones, light)
Characteristics of Trimeric G Proteins
- anchored in the cytoplasmic face of plasma membrane by lipids - 3 subunits (alpha, beta, gamma) - beta associates with gamma and gamma is linked to membrane -alpha is also linked to membrane and alternates between GTP and GDP states
What are the three different classes of microtubules that make up the mitotic spindle?
- astral microtubules - kinetochore microtubules - interpolar microtubules
Inhibitors of Apoptosis (IAPs)
- bind and inhibit activated caspases - Anti-IAPs prevent IAPs from binding caspases
RTK signaling via Ras
- binding of signal molecule - cross phosphorylation of RTK - Phosphate on RTK binds to an adaptor protein that recruits Ras GEF close to the plasma membrane - Ras GEF allows the inactive Ras protein to gain a GTP and become active
Prometaphase
- breakdown of nuclear enevelope
Describe the negative feedback loop associated with PKA and Phosphodiesterase
- cAMP binds to the regulatory subunits of PKA which activates the catalytic subunits - The catalytic subunits phosphorylate and activate cAMP phosphodiesterase which decreases production of cAMP
Regulation of Signaling by Proteolysis: Wnt/beta-catenin Signaling without Wnt
- can't bind to frizzled or co receptor LRP - complex of APC, axin, GSK3, and CK1 phosphorylate beta-catenin resulting in its degradation in proteasomes. - Wnt target genes are turned off
Tumor Microenvironemnt
- cancer cells - stroma: connective tissue containing a variety of cell types (fibroblasts, white blood cells), and endothelial cells of blood and lymphatic systems - stromal cells evolve to support cancer cells
Cancer and Replicative Cell Senescence
- cell division counting mechanism - depends on the shortening of telomeres - provides a built-in limit to number of times a cell divides - cancer cells get around this in two ways 1. keep tolemerase active so telomeres don't shorten or use another mechanism to elongate chromosome ends 2. disable checkpoints, cell cycle proceeds
Necrosis
- cells swell and burst in response to insult - more damaging to surrounding cells
Cancers arise from a single cell
- cells within the tumor share common chromosomal abnormalities (translocations), genetic mutations (point mutations), or epigenetic changes
What is the purpose of the G2/M checkpoint in the cell cycle?
- checking if environment is favorable - checking if all DNA is replicated - determines if cells can proceed into mitos
What is the function of the metaphase-anaphase checkpoint in the cell cycle?
- checks if all chromosomes are attached to the spindle - determines whether the cells should trigger anaphase and proceed to cytokinesis
What is the purpose of the start checkpoint in the cell-cycle?
- checks if the environment is favorable - do we have enough nutrients to support more cells - do we need more cells - determines if cells should enter the cell cycle and proceed to s phase
Metaphase
- chromosomes align at equator of spindle between the poles - chromosomes attach to the spindle
Telophase
- chromosomes arrive at the poles of the spindle and decondenses - nuclear envelope reassembles
Assembly and Contraction of the Contractile Ring
- composed of actin filaments and myosin filaments - myosin will constrict and allow for contractile ring to pinch these two cells - inactive RhoA becomes active by RhoGEF - Active RhoA helps to promote the assembly og the actin filaments and the activation of myosin to promote the contraction events needed to separate the cells
Role of M Phase
- consists of mitosis and cytokinesis - segregation of the correct number of chromosomes - production of daughter cells
How is Cdk regulated by cyclins?
- cyclin attaches to the T-loop of Cdk - Cdk-activating kinase phosphorylates t-loop resulting in fully active Cdk
CDK
- cyclin-dependent kinases - activities rise and fall throughout the cell cycle but levels remain the same.
What regulate the activity of CDK
- cyclins - direct CDks to target proteins - protein levels rise and fall throughout the cell cycle due to transcription and degradation.
Cytokinesis
- cytoplasm is divided in two by the action of the contractile ring
Characteristics of Apoptosis
- cytoskeleton dissassembly, breakdown of nuclear envelope, and DNA is cleaved - depends on cascade of degradation enzymes called caspases
What are the different ways we can transform a proto-oncogene to an oncogene
- deletion or point mutation in coding sequence - regulatory mutation - gene amplification - chromosome rearrangement
What are some of the rules that cancer breaks?
- does not commit to apoptosis if damaged - does not properly communicate with its neighbors - use up a lot of glucose, do not respond to signals in way that they should, proliferate uncontrollably causing tumors
Mechanisms of gene inactivation
- epigenetic gene inactivation - DNA is packaged in heterochromatin and not accessible for transcription - DNA methylation of c nucleotides and not accessible for transcription
Epinephrine Signaling Pathway
- epinephrine binds to G-protein-coupled receptor (adrenergic) - activates adenylyl cyclase promoting production of cyclic AMP - cAMP activates PKA which phosphorylates an inactive phosphorylase kinase and activates it - Phosphorylase Kinase phosphorylates glycogen phosphorylase resulting in its activation. - resulting in glycogen breakdown
Initiation of Mitosis
- fully inactive Cdk complex from CAK, Wee1, and M-Cyclin - Cdc25 removes the inhibitory phsophate and activates the M-Cdk
Anti-apoptotic Bcl2 proteins
- help to hold intrinsic pathway inactive - maintain membrane integrity to prevent the release of cytochrome c - inhibit class of proteins composed of Bax/Bak (transmembrane proteins in the outer mitochondrial membrane
Mutations in Tumor Suppressor gebe
- hereditary retinoblastoma
Notch signaling and Lateral Inhibition
- important in cell specification
Viruses and Tumor Progression
- in the presence of HPV 1. HPV can inject DNA into host cell but remain seperate resulting in benign growth or wart 2. HPV DNA can be injected and integrated with the host cell's chromosome resulting in a malignant tumor
What is the purpose/function of Myc
- increases expression of G1 cyclins - results in increased active G1-Cdk
Inactivation of signaling protein
- inhibitory proteins bind to an intracellular signaling protein in pathway to inactivate the pathway
Caspase Activation during Apoptosis
- initiator caspases and executioner caspases - apoptotic signal activates adaptor proteins on the initiator caspase which bring the initiator caspases together leading to dimerization, activation, and cleavage - initiator caspases target executioner caspases and cleave and activate them - Active executionar caspases can lead to cleavage of multiple substrates and apoptosis
Hormones are what kind of signaling molecules?
- intracellular - bind to DNA to regulate transcription of target genes
PI-3K-Akt Signaling and Cell Survival
- ligand is an insulin-like growth factor - PI-3K binds to a phosphate on rtk - PI-3K activated PIP2 which then Activates PIP3 - PIP3 binds to both PDK1 and AKT but PDK1 and mTOR phosphorylate and activate AKT - Active AKT leaves PIP3 and phosphorylates Bad Bad is inactive and releases an active apoptosis inhibitory protein - leads to the inhibition of apoptosis therefore promoting cell survival
How do you use the FRET technique?
- link Ras protein and GTP to dyes that will be activated by different wavelengths of light
Mitogens pathway to stimulate cell proliferation, activate Ras/MAPK pathway, and promote expression of immediate early gene expression
- mitogen binds to mitogen receptor - mitogen receptor activates RAS - Ras activates MAPKKK, MAPKK, and MAPK - MAPK phosphorylates and activates gene regulatory proteins - stimulates the transcription of target gene (immediate early gene) Myc - Myc binds and activates delayed response genes
Interpolar Microtubules
- move relative to each other during anaphase with the help fo kinesin motor proteins that are linked to the microtubules
Tumor progression
- multiple mutations are required to convert a healthy cell to a cancer cell - mutations can be present due to - inheritance - chemical carcinogens - radiation - errors in DNA replication - defects in DNA repair
How can the gene Myc lead to cancer
- overall our cells prevent cancer by inhbiting MDM2, leading to the production of p53 which leads to apoptosis - excessive Myc can lead to cancer if there are mutations in p53 and it cant activate it
How do we remove the Cdk inhibitor proteins when the error in the cell is fixed?
- proteolysis - active SCF complex phsophorylates CKI - ubiquitin and ubiquitylation enzymes form a polyubiquitin chaing on the CKI - Promotes degradation of CKI in a proteasome
Pathway involving cytokines
- receptors associate with cytoplasmic kinases (Janus kinase) - activated JAKs cross phosphorylate each other and phosphorylate receptors on the tyrosines - After Stats dock on the phosphates (SH2 domain), JAKs phsophorylate them - STATS dissociate and dimerize via SH2 domain - STATS translocated into nucleus, bind to DNA and other gene regulatory proteins to activate gene transcription
Properties of Cancer cells
- reproduce despite restraints on cell growth and division - invade local tissue and can colonize foreign location (metastasize)
Intracellular Receptors
- require the ligand to diffuse through the membrane - ligands need to be small and hydrophobic
Steps to Metastasis
- requires disruptions in cell-cell and cell-matrix adhesion (epithelial to mesenchymal transition)
Chronic Myelogenous Leukemia (CML)
- results from chromosomal translocation event - combines Bcr gene on chrom 22 with Abl gene on chrom 9 - Gleevec is able to bind to Bcr-Abl and inhibit its ability to produce a cell proliferation promoting signal - more of a treatment to keep the individual more healthy
What happens during Anaphase A
- shortening of the kinetochores - movement of daughter chromosomes to poles - forces generated mainly at kinetochores
GPCRs linked to Phospholipase
- signaling molecule activated GPCR - GPCR activates G protein - G protein (beta/gamma) will bind and activate phospholipase C - phospholipase C will cause a cleavage event of inositol phsopholipid into diacylglycerol (associated with membrane) and inositol 1,4,5 triphosphate (in cytosol) second messenger molecules - IP3 binds to a calcium channel embedded in the membrane of the ER resulting in the opening of the channel and the flow of calcium out of the ER lumen into cytosol - Calcium and diacylglycerol activated Protein kinase c
overactivity mutation (gain of function)
- single mutation event creates oncogene and promotes cell transformation - EX: Myc and Ras
Prophase
- sister chromatids condense - mitotic spindle begins to form outside nucleus
Anaphase
- sister chromatids separate and are pulled toward the spindle poles - kinetochore microtubules shorten and spindle poles move apart
What happens during Anaphase b?
- sliding force between interpolar mts push the poles apart - pulling force acts directly on the poles to move them apart
Strategies for Treating Cancer
- sooner you can eliminate cancer, the better - can treat with only one drug, but that can develop resistance to all of the drugs and uncontrollable cancer - can treat with a cocktail of drugs to maybe cause all of the cells to undergo cell death at once
How and when does centrosome duplication occur
- triggered by G1/S-Cdk - occurs during S phase
What is the Role of the M-Cdk Complex?
- triggers assembly of condensin complexes for chromosom condensation - induces separation of centrosomes and assembly of the mitotic spindle - ensures correct attachment of sister chromatids to the spindle - breakdown of nuclear envelope in animal cells
Tumors induce Angiogenesis
- tumors secrete signals that attract endothelial cells for growth of blood vessels to the tumor - tumors require blood vessels to supply nutrients and oxygen to survive
What is a way we can reduce the level of cAMP in the cell if the preceding g-protein is not activated?
- use cAMP Phosphodiesterase to convert cAMP into 5' AMP
Chromosomes pulled towards spindle poles
- uses energy from GTP hydrolysis occurring on tubulin subunits
Signaling Downstream of G Proteins
-AC= Effector Enzyme -1 G Protein activates 1 adenylyl cyclase (AC) -Stimulatory G Proteins (Gs) activate AC -Inhibitory G Proteins (Gi) inhibit AC -AC catalyzes the production of cyclic AMP (cAMP) from ATP -cAMP activates Protein Kinase A (PKA)
What happens if DNA is damaged?
-phosphorylation of p53 - Active p53 stimulates trancription of p21 (CKI) - results in cell cycle arrest because p21 inhibits G1/S and S cyclin complexes
What are the types of ligands
1) Cell surface bound 2) Secreted and bind cell-surface receptor 3) Hydrophobic and bind intracellular receptors
What are the three types of cell surface receptors?
1) Ion channel-coupled receptors 2) G-protein-coupled receptors 3) Enzyme-coupled receptors
What are the two positive feedback pathways in the initiation of mitosis?
1) M-cdk complex phosphorylates Cdc 25 to keep it active 2)M-Cdk complex phosphorylates Wee1 kinase to turn it off
What are the two types of Cancer-Critical Genes?
1) Overactivity mutation (gain of function) 2) Underactivity mutation (loss of function)
What are the two types of Enzyme-Coupled Receptors?
1) Receptor Tyrosine Kinases 2) Tyrosine-kinase associated receptors
One signal molecule can have varied responses due to ...
1) different receptors 2) different intracellular signals
What are the four forms of intercellular signaling?
1. Contact-dependent 2. Paracrine 3. Synaptic 4. Endocrine
3 Survival Factors Inhibit Apoptosis
1. Increased Production of anti-apoptotic Bcl2 protein 2. Inactivation of pro-apoptotic BH3-only Bcl2 protein - Bad = BH3 only protein 3. Inactivation of ant- IAPs - HID = anti-IAP
What are two possible ways tumors can form?
1. increased cell division/ normal apoptosis 2. Normal cell division and decreased apoptosis
Examples of Intracellular Receptors
Ach promotes the production of NO - NO binds/activates guanylyl cyclase - cGMP relaxes smooth muscle, allowing blood vessel to dilate - Viagra phosphodiesterase inhibitor keeps cGMP high
Inactivation of CREB
Activated by phosphorylation by a protein kinase - inactivated by dephosphorylation by a protein phosphatase
Mitogens
An extracellular signal molecule that stimulates cell division.
Which of the following mechanisms would not effectively decrease signaling in the PI-3K-Akt signaling pathway A. Endocytosis of the insulin-like growth factor B. Dephosphorylation of Akt C. Dephosphorylation of PIP3 D. Phosphorylation of Bad
B. Phosphorylation of Bad
Bax/Bak proteins are also called
BH123 proteins
contact-dependent signaling
Both the signaling cell and the target cell must be in close contact because they are both membrane bound molecules.
Regulation of Singaling by Proteolysis: Notch Signaling
Delta signal protein binds to the delta receptor (notch) (contact-dependent activation) - plasmic portion of the delta receptor breaks off, binds to DNA, promoting the transcription of notch responsive genes
Endocrine Signaling
Endocrine cell releases hormones that are transported in the blood stream to the receptor on the target cell.
True or False: In the epinephrine signaling pathway, when cAMP binds and activates PKA, amplification occurs
False
True or False - The Anaphase Promoting Complex promotes the degradation of the S-cyclins.
False, the APC promotes the degradation of M-cyclins
22. True or False: a proto-oncogene is characteristic of anything that inhibits the cell cycle (examples: Rb, p16, p53, Wee1 Kinase)
False, tumor surpressor genes inhibit the cell cycle
What are the four cyclins that function in the cell cycle?
G1-CDK G1/S-CDK S-CDK M-CDK
G1 cyclins regulate
G1/S cyclin
What are the three checkpoints within the cell cycle?
G2/M Metaphase to Anaphase Enter to S phase
Are trimeric G proteins in the active state when they are bound to GDP or GTP?
GTP
What is the purpose of GAP
GTP hydrolysis and turns the signaling molecule off
Hedgehog signaling when hedgehog molecule is present (HH)
HH binds to PTCH - PCTH inhibits smoothened (SMO) - alters the hedgehog signaling complex so GLI does not get cleaved - GLI dissociates from complex, binds to DNA and activates target gene transcription
What are the two main parts of the cell cycle?
Interphase and M phase
What does MAPK stand for?
Mitogen-activated protein kinase
Underactivity Mutation
Mutation event inactivates one tumor suppressor gene with one unaffected. The second mutation event inactivates second gene copy eliminating the tumor suppressor gene promoting cell transformation. EX: Rb, p53
Cancer Cell Accumulate Mutations
Mutations are accumulated at a higher rate than in normal cells in part due to inability to repair DNA damage or undergo proper chromosome segregation
What is one of the targets of activated PKA and what is the result?
PKA targets inactive CREB, phosphorylates it causing it to activate and bind to the activated target gene to promote gene transcription.
What is the other function of PKB
PKB stimulates movement of glucose transporter GLUT4 from internal membrane vesicles to the plasma membrane increasing the uptake of glucose
What is the process in which bacteria communicate called?
Quorom sensing
Short-lived Activation of Ras
Ras activation monitored by FRET (fluoresecence resonance energy transfer)
What are the two proteins viral proteins interfere with?
Rb and P53 - viral protein E7 binds to Rb and inhibits Rb. EF2 becomes active and will produce the cyclins needed for the progression through the cell cycle - viral protein E6 binds and inhibits p53 inhibiting the production of p21 and Cdk complexes will remain active
What is the main target for the G1-Cdk complex
Rb protein
Receptor Inactivation
Receptor remains at the surface and a protein binds to it so the intracellular domain of the receptor can no longer activate the next molecule in the pathway
Receptor Sequestration
Receptors are moved to an intracellular compartment (endosome) away from ligand to be held there
Paracrine signaling (neighbor stimulation)
Signaling cell releases signaling molecule that can diffuse from the cell and bind to nearby target cells.
Overactivity Mutation
Single mutation event that creates an oncogene that promotes cell transformation EX: Myc, Ras
Second Messenger
Small intracellular signaling molecule generated or released in response to an extracellular signal. Examples include cAMP, IP3, and Ca2+.
What is the function of protein kinase?
To add phosphate groups onto proteins
ion channel coupled receptors
Transmembrane receptor protein or protein complex that opens in response to the binding of a ligand to its external face, allowing the passage of a specific inorganic ion through the plasma membrane.
True or False: Nuclear receptors are activated by hormones and regulate gene transcription
True
What is an amplification event?
When a GPCR can activate mutliple G-proteins - enzyme catalyzed reactions - binding event that has to be maintained is NOT an amplification event
Synaptic signaling
a nerve cell releases neurotransmitter molecules into a synapse, stimulating the target cell
For the Wnt/B-catenin signaling pathway, in the absence of functional B-catenin, which of the following is NOT true? a. B-catenin are absent due to degradation via dephosphorylation b. Wnt target genes are turned OFF c. No transcription of the Wnt genes occur d. Ubiquitins were added to B-catenin, which sent it to the proteasome for degradation
a. B-catenin are absent due to degradation via dephosphorylation
19. When a cell receives an apoptotic signal, leading to the production of BH3-only proteins, what will occur right after? a. BH3-only inhibits anti-apoptotic Bcl2 proteins and therefore, cell death will not be inhibited b. BH3-only will activate anti-apoptotic Bcl2 proteins, enabling cell death c. Cytochrome C will stay in the mitochondria d. Effector Bcl2 proteins aggregate, allowing the cell to survive
a. BH3-only inhibits anti-apoptotic Bcl2 proteins and therefore, cell death will not be inhibited
What protein is responsible for making the M-Cdk complex inactive until conditions are right for mitosis? a. Wee1 Kinase b. Cdc25 phosphatase c. Myc d. E2F
a. Wee1 Kinase
The role of Adenyl Cyclase (AC) in the downstream signaling of G Proteins is: a.Converts ATP into cAMP, which activates Protein Kinase A (PKA) b.Directly activates Protein kinase A by a binding event c.Adenyl Cyclase binds to the extracellular signaling molecule d.Adenyl Cyclase binds to an intracellular signaling molecule
a.Converts ATP into cAMP, which activates Protein Kinase A (PKA)
kinetochore microtubules
attach to chromatids via kinetochores - shorten during anaphase
What class of proteins have protein levels that cycle throughout the cell cycle? a. Cdk's b. Cyclins c. Both cyclins and Cdk's d. Neither cyclins nor Cdk's
b. Cyclins
Which of the following is NOT true of Positron Emission Tomography? a. It measures glucose consumption/uptake by cells b. If oxygen is present, our cells will produce lactate; if oxygen is absent, our cells will undergo oxidative phosphorylation c. Tumor cells take up more glucose than healthy, normal cells do - this is measured on the PET
b. If oxygen is present, our cells will produce lactate; if oxygen is absent, our cells will undergo oxidative phosphorylation
During what phase of the cell cycle do chromosomes align at the equator-mitotic spindle? a. Prophase b. Metaphase c. Anaphase d. Telophase e. Cytokinesi
b. Metaphase
Endocrine Signaling is characterized by all of the following EXCEPT: a.Slower response due to diffusion in blood b.Ligands act at higher concentrations c.Receptor has a high affinity for ligands d.Ligand can travel farther distances
b. ligands act at higher concentrations
Which of the following is NOT true for p53? a. p53 is a tumor-suppressor gene b. p53 is rarely seen to be mutated in many cancer types c. p53 can be activated when DNA damage occurs, too much Myc, poor cellular conditions, or telomere shortening d. p53 inhibits the cell cycle
b. p53 is rarely seen to be mutated in many cancer types
Which of the following is NOT a mechanism for decreasing a G Protein Signaling Pathway? a.Activation of Phosphodiesterase b.Phosphorylation of the G Protein c.Phosphorylation of the GPCR
b.Phosphorylation of the G Protein
What is the purpose of GEF
binds GTP and turns signaling molecule on
Which of the following is NOT a cyclin-Cdk complex that exists in our bodies? a. G1cyclin-Cdk b. G1/S cyclin-Cdk c. G2/M cyclin-Cdk d. S cyclin-Cdk e. M cyclin-Cdk
c. G2/M cyclin-Cdk
This type of intercellular communication refers to the stimulation of neighboring cells. a.Endocrine b.Autocrine c.Paracrine d.Signal Transduction
c. Paracrine
In the "JAK-STAT" signaling pathway, which of the following does NOT occur? a.The receptors dimerize as a result of binding of a cytokine b.JAK molecules cross phosphorylate each other c.Amplification occurs resulting in an activated PKA molecule. d.After STAT molecules dock on specific phosphotyrosines on the receptors, the JAKsphosphorylate them
c.Amplification occurs resulting in an activated PKA molecule.
How does cAMP activate PKA?
cAMP binds to the regulatory subunits causing a conformational change which releases the catalytic subunits, activating them.
Carcinomas
cacncers in epithelial tissues (internal cavities) - predominates in the US
Positron Emission Tomography (PET) in detecting cancer
cancer cells have increased glucose uptake and metabolism, making it possible to visualize them with radioactively labeled glucose
Leukemias and Lymphomas
cancers in blood cells
Sarcomas
cancers in connective and muscle tissues
Programmed Cell Death
cells kill themselves in a controlled way
What is the function of condensins?
chromosome condensation
intercellular signaling
communication between cells
Intracellular Communication (Signal Transduction)
conversion of one signal to another (radio signal in, sound out)
What is the function of quorum sensing?
coordinates cell behaviors for things like motility, virulence, or antibiotic production
What are some of the diseases caused by mutations in the hedgehog signaling pathway?
cyclopia cleft palate defects in brain development loss of olfactory lobes carcinoma
What is an example of a Tyrosine Kinase Associated Receptor?
cytokine receptor
Which of the following events would NOT cause an increase in apoptosis? a. Release of cytochrome C from the mitochondria b. Binding of Fas ligand to its receptor c. Activation of BH3-only proteins d. Activation of Bcl2 e. Production of anti-IAPs
d. Activation of Bcl2
Which of the following could lead to the triggering of the intrinsic pathway of apoptosis? a. DNA Damage b. Insufficient oxygen/nutrients c. Lack of survival signals d. All of the above
d. All of the above
Which of the following are ways that a cell can have different responses in different cell types? a.Different amounts of the signaling molecule (morphogen) b.Different receptors for the same protein c.Different intracellular signaling proteins functioning in response to that signalingmolecule d.All of the above are true.
d. All of the above are true
Which of the following is NOT true when comparing Mitosis and Meiosis? a. Mitosis = occurs in somatic cells; Meiosis = occurs in germ cells b. Mitosis = same number of chromosomes as starting cell; Meiosis = half the number of chromosomes as the starting cell c. Mitosis = function is mainly for growth and repair; Meiosis = function in sexual reproduction d. Both mitosis and meiosis have homologs that are associated until Anaphase I
d. Both mitosis and meiosis have homologs that are associated until Anaphase I - for mitosis, homologs are NOT associated
In the insulin signaling pathway, which of the following molecules is activated by binding to IRS-1 (insulin receptor substrate - 1)? a.PIP3-dependent protein kinase (PDK1) b.Protein Kinase B (PKB) c.Glucose (Glc) d.Phosphoinositide-3-kinase (PI-3K)
d.Phosphoinositide-3-kinase (PI-3K)
What is the function of cAMP Phosphodiesterase (PDE)?
destroys cAMP by converting the active cAMP to an inactive 5' AMP to stop signaling
20. What are some of the ways that a healthy cell can be converted into a cancerous cell? a. Chemical carcinogens in the environment b. Radiation c. Errors in DNA replication or DNA repair d. Genetically inherited e. All of the above
e. All of the above
What does AC stand for in signaling
effector enzyme
What are the defects associated with hedgehog signaling?
extra denticles in drosophila
Morphogens
extracellular signaling molecules that causes cells to have different fates based on their level of exposure to the signal
Ultimately, quorum sensing affects the _________ _________________ of a cell
gene expression
What are scaffolds and what is their function?
hold proteins that function in a single pathway increasing the speed, efficiency, and specificity fo the pathway
What are the function of Cohesins
hold sister chromatids together along their length following the DNA replication that occurred in S-phase
Regulation of the Cyclin-Cdk Complex by Protein Binding
if there is an error that needs to buy the cell some time - Active Cdk/cyclin complex triggers the production of a Cdk inhibitor protein (CKI) like p27 and will bind to the complex making it temporarily inactive
Production of inhibitory protein
inhibitory protein that binds to the receptor preventing the activation of the next step in the pathway
Why are tyrosine-kinase associated receptors important?
it is conserved - required for cell proliferation, death, migration, and other functions
Ligands
molecules that stimulate a response in the target cell
What is G2 known as in the cell cycle?
monitoring phase
Underactivity Mutation (loss of function)
normal cell - mutation event in normal cell inactivates the tumor supressor gene in one gene copy - second mutation event in second gene copy - two inactivating mutations eliminate the tumor supressor genes and promote cell transformation EX: Rb, p53 (Inhibition of Rb or p53 prevents the stopping of the cell cycle)
What is the structure of Protein Kinase A?
normally an inactive tetramer with 2 regulatory and 2 catalytic subunits
specification
process of cells assuming specific functions during development
How is cAMP produced?
produced from ATP using adenylyl cyclase
survival factors
promote cell survival by suppressing apoptosis
What does cAMP bind to?
protein kinase A
Astral Microtubules
radiate outward toward the cell membrane
What is the speed of synaptic signaling?
rapid response ligand acts at high concentrations receptor has low affinity for ligand
Receptor Down-Regulation
receptor proteins are moved to the lysosome for degradation
Ca2+ Second Messenger
see image
Cooperative Regulation of the Cell Cycle
see image
Determining Protein Order in a Pathway
see image
Differences between mitosis and meiosis
see image
Easy/Difficulty in Metastasis
see image
Gamete production in mitosis and meiosis
see image
Insulin activation leading to glucose uptake and glycogen synthesis
see image
More complex differences between Mitosis and Meiosis
see image
Speed of signaling response
see image
Steps in Cell Cycle Arrest
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Steps in metaphase to anaphase transition
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Steps of Checkpoint 1
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Steps of Checkpoint 2
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Treating Cancer Now
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Typical Cell signaling pathway
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Ways Cyclin-Cdk complexes are regulates during the cell cycle
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Why Cell Death
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p53 tumor suppressor
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Progression of colorectal cancer
see image - APC is responsible for degradation of b-catenin
What is the speed of endocrine signaling?
slow response ligand acts at low concentrations receptor has high affinity for ligand
Name four processes in which cell communication is important
specification, cell mating, cell division, cell death
growth factors
stimulate the growth and division of cells
What is the function of protein phosphatase
to remove phosphate groups from proteins