MMG 409 Unit 3

What evolutionary advantage does SARS-CoV-2 gain from targeting the ACE2 receptor?

- ACE2 transports neutral amino acids, and recognizes neutral amino acids in the spike protein. - ACE2 has a protease activity that cleaves the viral spike protein and thus makes the subsequent fusion conditional, avoiding false negative reactions.

Viruses have evolved a number of strategies to escape from triggering the innate immune system response and counteracting its effects. Which innate immune systems are most important for viruses to evade or inhibit?

- Pattern Recognition Receptors such as Toll-like receptors - Type I Interferon response

What are the consequences for mutated and/or overexpressed cyclin D or E levels for cancer cells?

- cell cycle checkpoints are no longer maintained and cells cycle faster than normal cells - DNA damage remains when entering S phase before cells move forward in the cell cycle - Damaged or incompletely replicated chromosomes may be haphazardously "repaired" through non-homologous end joining leading to chromosomal aberrations

Individuals substantially reduce their cumulative risk of dying from lung cancer by stopping smoking. Why

- the tumor promoting effect of tobacco smoke ceases to drive cancer cell proliferation. - the lowered mutagenic load also reduces the chance of acquiring mutations in genes that drive lung cancer. - When smoking ceases, the chronic wound healing process also gradually stops.

What types of vaccines against SARS-CoV2 have been developed to prevent severe disease and hospitalization from COVID19?

-modified mRNA containing the S gene delivered in lipid nanoparticles - adenoviral vectors in which the E3 gene is replaced by the S gene of SARS-CoV2 - whole inactivated virus treated with beta propriolactone to crosslink proteins and nucleic acids and prevent the virus from replicating - subunit vaccines of purified Spike protein or the Spike receptor binding domain (RBD) peptide mixed with lipid nanoparticles for delivery

The MHC-class 1 and 2 presentation systems offers advantages over the innate PAMP receptor and complement pathways. Which of the statements below are correct? 1. PAMP receptors recognize constant features of invading pathogens, and viruses may evolve to not trigger or to inactivate them. 2. Presentation of digested internal proteins on MHC class I provides a sampling of all cellular and viral proteins, whereas only viral surface protein(s) - which are usually the most variable - would trigger a reaction by PAMP receptors (e.g. TLR 2, 4,5), or complement, which is considerably more limited in scope. 3. Alarm signaling through the MHC-class 1 and 2 presentation depends on PAMP receptor signaling and thus provide a second (co-stimulatory molecules) and third signal (stimulatory cytokines).

1, 2, and 3 are correct.

Which of the following gene products and their corresponding pathways are downstream effectors of Ras signaling and result in what outcomes? 1. Raf » MAPK pathway: Erk1/2 » shuttles into nucleus and phosphorylates nuclear proteins involved in cell proliferation, including cyclin D1 2. PI3-Kinase » Wnt pathway: phosphorylates GSK3beta » beta catenin no longer degraded and can move to the nucleus where it induces TP53 gene expression (encoding p53) 3. PI3-Kinase » activates second messengers with PH domain » Akt/PKB, Rho-GEFs » Akt phosphorylates Bad (blocks apoptosis) and p21, p27 (locate to cytoplasm, no longer bind to CDKs and no longer block cell cycle progression) 4. Ral-GEFs » activate Ras-like proteins A and B (RalA and RalB) by replacing their GDP with GTP » activate a collection of different effectors affecting cytoskeleton and motility, transcription, cell survival and proliferation Ral-GAPs » inactivate Ras-like proteins A and B (RalA and RalB) » promote apoptosis as a safety mechanism

?

What evolutionary advantage does SARS-CoV-2 gain from targeting the ACE2 receptor?

ACE2 is highly expressed on respiratory tract and gut epithelial cells, two favorite virus target tissues and ACE2 has a protease activity that cleaves the viral spike protein and thus makes the subsequent fusion conditional, avoiding false negative reactions.

Which of the following is NOT a mechanism used to regulate cyclin-Cdk complexes? Acetylation Inhibitory protein binding Polyubiquitinylation Phosphorylation

Acetylation

The contractile ring performs the essential function to pull the midplane cell membrane together and subsequently split the mitotic cell into two daughter cells. This structure consists of which cytoskeletal components?

Actin and Myosin

M-Cdk activation throughout the cell can occur rapidly due to positive feedback loops. Which of the following statements is an accurate description of how these positive feedback loops function?

Active M-Cdk can negatively regulate the activity of the inhibitory kinase Wee1 and activates Cdc25 phosphatase

Motor proteins perform which of the following functions during mitosis? Positioning the centrosomes at the poles Maintaining centrosome positioning in the cell relative to each other Moving sister chromatids to the metaphase plate All of the above None of the above

All of the above

The pro-apoptotic Bcl2 family proteins Bax and Bak are localized to the outer membrane of the mitochondria can form a channel called the Mitochondrial Apoptosis-Induced Channel (MAC) to promote apoptosis. How is the formation of this activity inhibited in the absence of apoptotic signals?

Anti-apoptotic Bcl2 family members such as Bcl2 prevent the aggregation of Bax and Bak in the absence of apoptotic signals

An important difference between apoptosis and necrosis is:

Apoptotic cells maintain membrane integrity and break down intracellular macromolecules while necrotic cells break open in an unregulated manner

Three models have been proposed to suggest how the contractile ring can be localized to the cellular midplane. The existing spindle structure remaining from mitosis is important in all of these models. Which of the following types of spindle microtubules are implicated in these models?

Astral microtubules and Interpolar microtubules

Alfred Knudson's "two hit hypothesis" for tumor suppressor genes (TSGs) states the following condition needs to be met for cancers to initiate and progress:

At least two alleles of a tumor suppressor gene on the maternal and paternal chromosome need to be "hit", i.e., inactivated by genetic and/or epigenetic mechanisms.

What are the critical signals that indicate proper biorientation of sister chromatids and thereby promote metaphase-to-anaphase progression?

Attachment of the kinetochores and tension between sister chromatids

How does the regulation of cyclin-Cdk complexes by inhibitory phosphorylations resemble the inhibition by the binding of CKIs?

Both forms of regulation directly interfere with the active sites of the Cdks and prevent the binding of substrates

How does Cdc25 promote the entry into mitosis

Cdc25 is a phosphatase that can remove only specific, Wee1 mediated phosphorylation on M-Cdk, and thereby activate it

What is an important difference between the G1 and G2 phases of the cell cycle?

Cells duplicate their genomic material after the G1 phase, and therefore have twice as much genetic material in the G2 phase

Origins are regulated to only fire once during every round of the cell cycle. Which of the following is NOT a mechanism that prevents the re-use of origins? ORC inactivation Inhibition of Mcm Helicase loading Cohesin loading Both a and b All of the above

Cohesin loading

Which of the following statements is NOT a true statement comparing cohesin and condensin? Both proteins are important for organizing re-structing genomic material for mitosis Both proteins share a similar structure, with two arms interacting through hinge domains with ATPase head groups Condensin functions primarily to hold sister chromatids together, while cohesin largely compacts the duplicated genomes All of the above statements are true

Condensin functions primarily to hold sister chromatids together, while cohesin largely compacts the duplicated genomes

Cdks possess the kinase activity required for cell cycle progression. What protein is required to both drive Cdk activation and specificity?

Cyclins

Cytochrome c is normally sequestered in the intermembrane space of mitochondria where is participates in the electron transport chain. However, it is also an important component of the intrinsic apoptotic pathway. What does cyctochrome c do in this pathway?

Cytochrome c activates Apaf1 to form a heptamer that promotes initiator caspase activation

What hold bivalents together during meiosis I?

DNA crossovers

One of the most common signals that can inhibit the action of cyclin-CDK complexes during the cell cycle is:

DNA damage

Which pathway(s) would be impacted by an amino acid exchange p53 mutation on S15 (site of ATMATR phosphorylation) -DNA damage response - Myc signaling pathway

DNA damage response

Which pathway(s) would be impacted by a p53 mutant that has decreased DNA binding affinity

DNA damage response and Myc signaling pathway

Apoptotic cells are often labelled using fluorescent dyes that can bind to free DNA ends. Why does this labeling technique specifically mark apoptotic cells?

Executioner caspases release the endonuclease CAD by cleaving its inhibitor iCAD, resulting in genomic degradation

Fas signaling is an example of the activation of an extrinsic apoptotic signaling pathway. How does Fas binding to the Fas Death receptor impact apoptosis in the target cell?

Fas binding recruits adaptors and initiator caspases into the Death Inducing Signal Complex (DISC) to drive caspase activation

Flow cytometry is a powerful tool for analyzing cell cycle progress in a population of cells. In what stage of the cell cycle are the cells in Peak 1 likely to be?

G1

Which phase of the cell cycle is indicated by the 1st peak on a cell count graph

G1

Which phase of the cell cycle is indicated by the 2nd peak on a cell count graph

G2 or M

RhoA GTPase is an integral to organizing and assembling the contractile ring. As a G-protein, RhoA is active when bound to ________ and this form of RhoA is promoted by the action of _________.

GTP; RhoGEF

Number of divisions cells (other than stem cells) can perform before they undergo senescence or apoptosis

Hayflick limit

Initiator caspases share a similar mechanism of activation. Which of the following statements best describes the activation of these caspases?

Inactive caspases are brought into close proximity, where they can cleave their partner caspase and form an active complex

Bcl2 family member proteins can function as either pro or anti apoptotic factors. They are characterized by the inclusion of one or more Bcl Homology (BH) domains. What is true about the BH homology domains?

Initiator caspases are activated by adaptor protein binding, which allows them to function as adaptor proteins for executioner caspases

What is the functional difference between interpolar microtubules and kinetochore microtubules?

Interpolar microtubules form anti-parallel associations with the opposing centrosome while kinetochore microtubules connect sister chromatids to spindle poles

Polar ejection force results in the arms of chromosome lagging behind the centromeres during anaphase. Loss of which of the following motor protein(s) would result in the loss of this "polar wind"?

Kinesin-4 and Kinesin-10

Most cells rely on a G1 phase to ensure the commitment to entering the cell cycle is only made when conditions are conducive to cell division. In order to maintain a G1 phase, M-cyclins must be suppressed. How do cells achieve this?

M-cyclins are initially degraded by the action of Cdc20-APC/C during M phase, which results in decreased Cdc20-APC/C activity. APC/C activity is maintained through the G1 phase by the expression of alternate partner Cdh1, preventing M-cyclin accumulation

What is a critical role of the synaptonemal complex?

Maintains maternal and paternal sister chromatids in close association to promote chiasma and crossovers

The Origin Recognition Complex (ORC) is one of the first protein factors that identifies and binds to an origin of replication. After the ORC is bound, the next critical functional component of the prereplicative complex recruited is:

Mcm Helicase

A critical cell cycle checkpoint occurs between which two mitotic stages?

Metaphase and Anaphase

Microtubule attachment to the kinetochore is critical for mitotic progression. How do microtubules interact with the kinetochore to facilitate sister chromatid segregation?

Microtubules are embedded in the kinetochore where they are bound by Ndc80 to link sister chromatids to the microtubules

Which pathway(s) would be impacted by the deletion of Arf1 -DNA damage response - Myc signaling pathway

Myc signaling pathway

How will growth factor signaling be impacted by a mutation to PI 3-kinase that leads to constitutive activation

PI3-kinase will drive cell growth even in absence of signal

Which of the following is a true statement about cell cycle checkpoints? Passage through checkpoints is irreversible The decision to move through checkpoints is based solely on extracellular conditions Cells can shift from G2 back to G1 if extracellular conditions are not supportive of mitosis Both a and b are true All of the above statements are true

Passage through checkpoints is irreversible

Survival signaling is required for cell survival because without the signals, cells actively:

Promote pro-apoptotic pathways

How would the mitogen signaling pathway be influenced by a Ras mutant that has lost GTPase activity

Ras would remain active independent of signal and drive the cell cycle forward

How would the mitogen signaling pathway be influenced by a Rb mutant that mimics constitutive phosphorylation

Rb would be inactive, leading to continuous E2F activation and cell division independent of mitogen signaling

Growth factor signaling through PI 3-kinase and TOR is an example of what type of cell signaling pathway?

Receptor Tyrosine Kinase Signaling

what happens to contractile ring formation and function in the presence of a RhoA mutant that inactivates the GTPase activity of the protein

RhoA will be active and form contractile ring components throughout the cell

Which phase of the cell cycle is indicated by the trough between the 2 peaks on a cell count graph

S

What would happen to S-Cdk activation if all but 2 phosphorylation sites on Sic1 were removed

S-Cdk would activate slower, as the low affinity binding sites would be a poor target for the SCF complex

In order for cells to advance from metaphase to anaphase, the cohesin rings holding sister chromatids together must be degraded. What protein is responsible for this action, and how is it regulated?

Separase cleaves the cohesin rings but is held in an inactive state by Securin until the APC/C activates

What happens to cellular materials during asymmetric cell division, and why is this an important mechanism?

Specific cytosolic components and organelles are divided unequally to allow for later differentiation of cells

Which of the following statements about the retinoblastoma gene and its gene product, pRb, are true (T) or false (F)? 1. The Rb gene product controls movement through the R point of the cell cycle. 2. The Rb protein is localized to the nucleus where it phosphorylates cell cycle proteins. 3. Un- and hypophosphorylated pRb binds to E2F transcription factors, thereby preventing the expression of E2F target genes whose products are needed for the S, G2, and early G1 phases of cell cycle. 4. The Rb protein blocks cell cycle progression past the R (reversibility) point unless it becomes completely dephosphorylated by cyclin A-dependent phosphatase.

TFTF

Which genes are part of the TGFB1 Pathway? - APC, DCC, TGFBR2 - TGFBR2, Smad2, Smad4 - Smad2, Smad4, Bax, p53 - all of the above

TGFBR2, Smad2, Smad4

Both the Anaphase Promoting Complex (APC/C) and the SCF complex help to advance cells through the cell cycle by targeting proteins for degradation by the proteosome. How do their mechanisms of action differ?

The APC/C is activated by binding with a protein partner that directs it to target proteins for degradation, while the SCF identifies target proteins when they are phosphorylated in order to direct proteins to the proteosome

How does the extrinsic pathway of apoptosis differ from survival signaling?

The extrinsic pathway uses receptor binding to direct a cell to enter apoptosis while survival signaling directs cells to prevent apoptosis

The synaptonemal complex forms between paired paternal and maternal sister chromatids to promote chiasma. What would happen during mitosis if the synaptonemal complex were to be maintained through metaphase I?

The paternal and maternal homologs would remain physically associated even after cohesin degradation

In the presence of DNA damage, cells inhibit progression through the cell cycle. How do the DNA surveillance proteins protein cell cycle arrest?

The phosphorylation of p53 stabilizes and activates it to drive transcription* of a CKI

Mitogens are extracellular signals that promote cell progression through the cell cycle. In the case of Ras GTPase activation, a signaling cascade promotes Myc expression and the phosphorylation of Rb. These cellular events promote what activities in the cell?

Transcription of pro-S phase proteins through Myc and E2F activation

What are two major ways in which survival signaling can inhibit apoptosis?

Transcriptional upregulation of anti-apoptotic proteins and activation of anti-apoptotic proteins

Test of biological agents, chemicals, or physical processes for their ability to induce a focus on cell monolayer

Transformation assay

T/F The earlier a cancer is diagnosed, the better are the chances for a cure.

True

Microtubule flux generates an important poleward force on sister chromatids during the M phase. What is happening at each end of the microtubule to maintain this flux?

Tubulin is removed at the - end of spindle microtubules while also being added at the + end, resulting in treadmilling

Which of the following statements about chemical carcinogenesis is incorrect? -A complete carcinogen has both mutagenic and tumor promoting activity. -Tumor initiation occurs upon acute exposure to a mutagenic chemical that damages the genomes of healthy tissue cells whereas tumor promotion involves the repeated / chronic exposure to tumor promoting chemicals that damage the tissue but do not alter the DNA sequence or structure. -Tobacco smoke contains multiple mutagens, tumor promoters and complete carcinogens. -Tumor progression occurs after acute exposure to a tumor promoting chemical that damages the genomes of healthy tissue cells whereas tumor initiation requires the chronic exposure to tumor promoting chemicals that damage the tissue but do not alter the DNA sequence or structure.

Tumor progression occurs after acute exposure to a tumor promoting chemical that damages the genomes of healthy tissue cells whereas tumor initiation requires the chronic exposure to tumor promoting chemicals that damage the tissue but do not alter the DNA sequence or structure.

Downstream effects of Ras signaling on Ral-GEFs results in what outcome

activate Ras-like proteins A and B (RalA and RalB) by replacing their GDP with GTP >> activate a collection of different effectors affecting cytoskeleton and motility, transcription, cell effectors affecting cytoskeleton and motility, transcription, cell survival and proliferation

Downstream effects of Ras signaling on Raf results in what outcome

activates MAPK pathway: Erk1/2 shuttles into nucleus and phosphorylates nuclear proteins involved in cell proliferation including cyclin D1

Downstream effects of Ras signaling on PI3-Kinase results in what outcome

activates second messengers with PH domain >> Akt/PKB, Rho-GEFs Akt phosphorylates Bad (blocks apoptosis) and p21, p27 (locate to cytoplasm, no longer binds to CDKs and no longer blocks cell cycle progression)

The initial response to injury and bleeding triggers the clotting cascade. Which of the following steps does not contribute to the acute wound healing response? - Epithelial-Mesenchymal Transition (EMT): Epithelial cells change from stationary to migratory state, detach from their neighbors and migrate into the wound site - adaptive immune cells, such as B and T cells, infiltrate the wound immediately to defend against bacterial infection and invasion - innate immune cells, such as macrophages, dendritic cells, and neutrophilic leukocytes, infiltrate the wound immediately to defend against bacterial infection and invasion - the fibrin clot that carries platelets and red blood cells/erythrocytes releases growth factors that stimulate the growth and proliferation of fibroblasts (FGF, PDGF), epithelial cells (EGF), and endothelial cells (VEGF)

adaptive immune cells, such as B and T cells, infiltrate the wound immediately to defend against bacterial infection and invasion

Mutations in cell cycle genes that can lead to cancer

all

Mortality due to lung cancer was followed in groups of males in the United Kingdom for 50 years. Figure 20-3 (slide 65) shows the cumulative risk of dying from lung cancer as a function of age and smoking habits for four groups of males: those who never smoked, those who stopped at age 30, those who stopped at age 50, and those who continued to smoke. These data show clearly that individuals can substantially reduce their cumulative risk of dying from lung cancer by stopping smoking. What do you suppose is the biological basis for this observation? A. The likelihood to develop and die from lung cancer is reduced becausethe tumor promoting effect of tobacco smoke ceases to drivecancer cell proliferation. B. Likewise, the lowered mutagenic load also reduces the chance of acquiring mutations in genes that drive lung cancer. C. When smoking ceases, the chronic wound healing process also gradually stops.

all of the above

ability of cells to grow without the requirement to attach to the extracellular matrix

anchorage independence

How would the intrinsic pathway of apoptosis be impacted by the introduction of a cytochrome c analog that mimics binding to Apaf1?

apoptosis would be induced even in the absence of any apoptotic signals

How would the intrinsic pathway of apoptosis be impacted by an Apaf1 mutant that constituitively forms a heptamer in combination with an over-expression of anti-apoptotic Bcl-2 family proteins

apoptosis would be inhibited by the Bcl-2 family proteins preventing downstream activation of apoptotic factors

when Cancer cells produces both its growth factor and GF receptor

autocrine loop

What occurs in cells in response to Fas ligand binding

binding forms the death inducing signal complex and promotes initiator caspase cleavage

TGF-beta when applied to epithelial cells has what downstream effect

binds to the heterodimeric TGF-beta receptor whose signaling induces expression of the inhibitory p15INK gene

What pathway is involved in survival signaling - Akt pathway - MAP kinase pathway

both

Which pathway(s) would be impacted by a peptide that competes with p53 for Mdm2 binding -DNA damage response - Myc signaling pathway

both

What is the growth phenotype seen when the Wee1 phosphorylation site on M-Cdk is mutated

cells are smaller, as the loss of the Wee1 regulatory site results in premature entry into mitosis

How would the intrinsic pathway of apoptosis be impacted by an initiator caspase that posesses a mutation that blocks cleavage in between the large and small subunit

cells would not be able to enter apoptosis as initiator caspases could not be cleaved and become active

How would the intrinsic oathway of apoptosis be impacted by Bcl-2 family members that possess a mutation that prevents aggregation in the outer mitochondrial membrane

cytochrome c would not be released from the mitochondrial membrane in response to apoptotic signals, inhibiting apoptosis

What explains the difference in DNA count data gathered from wild type cells and cells with unstable securin

early loss of securin leads to uneven distribution of sister chromatids, and the resulting cells have abnormal chromosome numbers

How would the mitogen signaling pathway be influenced by a Myc mutant that cannot be degraded

excessive accumulation of Myc will result in activation of p53 and either cell cycle arrest or apoptosis

T/F Alcohol prevents cancer since in sufficient dose it kills tumor cells

false

T/F ORF8 variant strains with reduced virulence may make good decoys for treatment of patients with severe COVID19

false

T/F The EGF receptor gene can be turned into an oncogene by activation of the RTK domain through dimerization with the myosin light chain

false

T/F The EGF receptor gene can be turned into an oncogene by deletion of its phosphotyrosine containing cytoplasmic domain so that it can no longer be activated

false

T/F The Rb protein blocks cell cycle progression past the R (reversibility) point unless it becomes completely dephosphorylated by cyclin A-dependent phosphatase.

false

T/F The Rb protein is localized to the nucleus where it phosphorylates cell cycle proteins.

false

T/F The p53 protein induces apoptosis by closing up the mitochondrial channels and thus depriving them of oxygen

false

T/F Toll-like receptors trigger a signaling cascade that results in the direct stimulation of immunoglobulin and T cell receptor genes in B and T cells, respectively, thus connecting the innate to the adaptive immune response

false

T/F Tumor progression occurs after acute exposure to a tumor promoting chemical that damages the genomes of healthy tissue cells whereas tumor initiation requires the chronic exposure to tumor promoting chemicals that damage the tissue but do not alter the DNA sequence or structure.

false

T/F binding of a GTPase activating protein (Ras-GAP) to Ras induces the Ras GTPase domain to hydrolyze GTP to GDP, resulting in an inactive Ras-GDP

false

T/F the following step contributes to the acute wound healing response: adaptive immune cells, such as B and T cells, infiltrate the wound immediately to defend against bacterial infection and invasion

false

T/F the variant ORF8 proteins fail because they do not fold correctly and no longer bind any IL17 receptor

false

T/F stem cells cannot divide for the entire lifetime of the organism

false, it can

T/F Src activation involves a switch from intramolecular domain interactions to intermolecular domain interactions, which liberates the tyrosine kinase domain to autophosphorylate the activation loop and thus become able to phosphorylate other target proteins

false... why??

What signaling effects does mutated and/or overexpressed Src have for cancer cells?

growth arrest and senescence

what does it mean when there is a breach of the basement membrane

hallmark of malignancy

If you introduce a mutant form of G1-cyclin that could allow G1-Cdk to target Sic-1, what phenotype would you expect?

inability to halt the cell cycle prior to the START checkpoint in G1, as G1-Cdk is active prior to the checkpoint

TGF-beta when applied to epithelial cells has the following downstream effects:

it binds to the heterodimeric TGF-beta receptor whose signaling induces expression of the inhibitory p15INK4B gene

What happens to contractile ring formation and function if the RhoA GAP is localized in the midplane

it will counteract the midplane RhoA GEF and result in decreased RhoA activity and inhibited contractile ring formation and contraction

How will growth factor signaling be impacted by a mutation to growth factor receptors that inactivates the kinase domain?

loss of the kinase activity prevents the transmission of the signal, preventing cell growth

Mutations in 2 important cancer-critical genes, TP53 and Rb encoding p53, and pRb, respectively, are commonly found in cancers. What types of mutations are associated with these genes?

loss-of-function mutations in 1 pTP53 allele and both alleles of Rb

What happens to contractile ring formation and function in the presence of a myosin light chain mutant that lacks the regulatory phosphorylation sites

myosin II cannot be activated, resulting in a failure to contract the contractile ring

What growth phenotype would you expect if you were to knock out both Wee1 and Cdc25?

small cells, as the loss of Wee1 results in active M-Cdk and early mitotic entry

What is the meaning of a peak shifting to the right over time in a cell count analysis of cell cycle

suggests increased DNA content from S phase synthesis

Why are mutant strains highly sensitive to a microtubule destabilizing drug benomyl

the spindle assembly checkpoint is compromised and cells enter anaphase prematurely

How can a wild type strain maintain viability even in the presence of the microtubule destabilizing drug benomyl

the wild type halts in mitosis in order to delay until biorientation is acheived

Loss of CDK inhibitors (tumor suppressor genes) through epigenetic silencing leads to cancer

true

Sporadic mutations in the Rb and TP53 (p53) gene leads to cancer

true

T/F A complete carcinogen has both mutagenic and tumor promoting activity

true

T/F A single mutation is NOT enough to turn a normal cell into a cancer cell

true

T/F Affinity to IL17RC does not appear to matter for triggering CCL20 and CXCL1 chemokine and IL6 cytokine production

true

T/F All coronaviruses have a common ancestor.

true

T/F All variants bind to IL17RA, but with decreasing affinity: wt>S24L>V62L>L84S

true

T/F Cancer can be induced by infectious agents such as viruses

true

T/F Cancer is largely, though not completely preventable except in families whose germline DNA carries mutations in tumor suppressor or DNA repair genes and who may be helped greatly by preventive surgery

true

T/F Coronaviruses have been transmitted across species barriers on multiple occasions.

true

T/F Given the mutation rate, a new ORF8 variant strain may emerge at any time that has acquired enhanced virulence

true

T/F Guanine nucleotide releasing protein (GNRP) (aka Ras-GEF) replaces GTP with GDP and inactivates Ras

true

T/F Interleukin 17 receptor blocking antibodies may be helpful in the treatment of COVID19

true

T/F Most Cancers originate from a single aberrant cell

true

T/F Mutations at the phosphorylation site of CDKs leads to cancer

true

T/F ORF8 variant strains with greatly reduced virulence may make good vaccines for preventing patients from developing severe COVID19

true

T/F Overexpression of cyclins through gene amplification leads to cancer

true

T/F Overexpression of promoting kinases through promoter mutation leads to cancer

true

T/F PAMP receptors recognize constant, non-specific features of invading pathogens fast, but viruses may evolve to not trigger or to activate them

true

T/F Peak binding to IL17RC is the same for wt ORF8 and the three variants

true

T/F Presentation of digested internal proteins on MHC class I provides a sampling of all cellular proteins, including those of viral origin, however viruses suppress MHC class I surface presentation of viral peptides

true

T/F T cell activation through MHC-class 1 and 2 antigen presentation (signal 1) depends on PAMP receptor recognition by antigen presenting cells, which also provide a second (expression of co-stimulatory molecules, B7-1/2) and third signal (stimulatory cytokines)

true

T/F The ACE2 receptor is conserved enough through evolution to serve as beta coronavirus receptor without major changes to the viral amino acid sequence and tertiary structure.

true

T/F The EGF receptor gene can be turned into an oncogene by deletion if its extracellular ligand binding domain and constitutive dimerization of the cytoplasmic domain leading to increased tyrosine kinase activity

true

T/F The EGF receptor gene can be turned into an oncogene by overexpression due to mutation in the promoter sequence

true

T/F The EGF receptor gene can be turned into an oncogene by overexpression due to placement under a heterologous promoter (chromosomal rearrangement)

true

T/F The MHC-class 1 and 2 presentation systems offers advantages over the innate PAMP receptor and complement pathways... Alarm signaling through the MHC-class 1 and 2 presentation depends on PAMP receptor signaling and thus provide a second (co-stimulatory molecules) and third signal (stimulatory cytokines).

true

T/F The MHC-class 1 and 2 presentation systems offers advantages over the innate PAMP receptor and complement pathways... PAMP receptors recognize constant features of invading pathogens, and viruses may evolve to not trigger or to inactivate them.

true

T/F The MHC-class 1 and 2 presentation systems offers advantages over the innate PAMP receptor and complement pathways... Presentation of digested internal proteins on MHC class I provides a sampling of all cellular and viral proteins, whereas only viral surface protein(s) - which are usually the most variable - would trigger a reaction by PAMP receptors (e.g. TLR 2, 4,5), or complement, which is considerably more limited in scope.

true

T/F The Rb gene product controls movement through the R point of the cell cycle.

true

T/F The presentation of peptides by MHC molecules enables the immune system to respond to the vast spectrum of proteins that viruses may encode but within the limitation of MHC class I and II binding

true

T/F The v-src gene of Rous Sarcoma Virus is a greatly modified version of the cellular src gene that encodes a serine-theronine kinase

true

T/F The wild type ORF8 protein triggers most CCL20, CXCL1, and IL6 production because it fully heterodimerizes IL17RA and IL1RC

true

T/F Tobacco smoke contains multiple mutagens, tumor promoters and complete carcinogens.

true

T/F Tumor initiation occurs upon acute exposure to a mutagenic chemical that damages the genomes of healthy tissue cells whereas tumor promotion involves the repeated / chronic exposure to tumor promoting chemicals that damage the tissue but do not alter the DNA sequence or structure.

true

T/F Un- and hypophosphorylated pRb binds to E2F transcription factors, thereby preventing the expression of E2F target genes whose products are needed for the S, G2, and early G1 phases of cell cycle.

true

T/F separate signals are required to drive proliferation and inhibit apoptosis

true

T/F the following step contributes to the acute wound healing response: Epithelial-Mesenchymal Transition (EMT): Epithelial cells change from stationary to migratory state, detach from their neighbors and migrate into the wound site

true

T/F the following step contributes to the acute wound healing response: innate immune cells, such as macrophages, dendritic cells, and neutrophilic leukocytes, infiltrate the wound immediately to defend against bacterial infection and invasion

true

T/F the following step contributes to the acute wound healing response: the core serum response (CSR) genes are induced or repressed for the first 24-48 hours in response to the growth factor stimulation

true

T/F the following step contributes to the acute wound healing response: the fibrin clot that carries platelets and red blood cells/erythrocytes releases growth factors that stimulate the growth and proliferation of fibroblasts (FGF, PDGF), epithelial cells (EGF), and endothelial cells (VEGF)

true

What would a DNA electrophoresis gel look like for a fraction that contains the survival signal (whole or degraded)

whole because the genomic DNA would not be processed by endonuclease