Cell Signaling

the voltage-clamp technique is uniquely able to keep which variable constant? I (Em-Erev) N Po Y

(Em-Erev)

Which single-channel patch clamp technique mimics a scenario where the void of the needle serves as the "inside" of the cells and the solution the tip of the needle is placed into serves as the "outside"? cell-attached recording whole-cell recording inside out recording outside out recording sharp needle recording

outside out recording

the latent TBF-B peptide must be cleaved by what protease in order to be activated? plasmin trypsin papain chymotrypsin PARP

plasmin

how many DNA binding domain do Smads have? 0 1 2 3 4

1

What is the relationship between oncogenes and proto-oncogenes? proto-oncogenes are more carcinogenic than oncogenes oncogenes promote cancer while proto-oncogenes inhibit cancer oncogenes become proto-oncogenes during carcinogenesis proto-oncogenes become oncogenes during carcinogenesis

proto-oncogenes become oncogenes during carcinogenesis

Toll-like receptors (TLRs) primarily activate which NF-kB signaling pathway? canonical non-canonical

canonical

Which is the proper order of activation in the MAPK signaling cascade? ERK --> MEK --> MEKK MEKK --> MEK --> ERK ERK --> MEKK --> MEK MEKK --> ERK --> MEK MEK --> MEKK --> ERK

MEKK --> MEK --> ERK

Find an FDA approved drug that targets a GPCR. What is its name, what receptor does it target, what disease does it treat, and how does it work?

Montelukast is a leukotriene receptor antagonist that targets GPCRs. It is used to treat asthma. This drug bind with high affinity and selectivity to the Cys LT type 1 receptor which inhibits the actions of CysLts at the receptor. This drug will help with asthma, bronchoconstriction, and seasonal allergies.

Describe TWO potential mechanisms by which IκB may prevent the NF-κB complex from being active. These don't have to be true; they simply have to be biologically plausible. I just want you to think about how systems like this work.

Two ways to prevent the complex from being active is either by using mutant forms of IkBs (SRs), which will bind to the NF-kB. The mutant forms cannot be phosphorylated or degraded. Also the phosphorylation of serine residues will lead to proteasomal degradation, which will result in the release of the NF-kB complex. - IkB binds Nf-Kb complex and prevents it from being active: -> one way to do this is blocking it from entering the nucleus -> prevent it from binding to the DNA

What is an advantage of measuring the opening and closing of a single channel rather than that of a population of channels?

Single-channel recording allows for high-resolution measurement of unique channel events. This allows one to see discrete jumps in conductance as the channel opens and return to normal as channel closes. You can also see the duration of channel opening and closing as well as the frequency of channel gating.

Which families of GPCRs contain disulfide bonds between the 1st and 3nd extracellular loops? select all that apply. Family A Family B Family C

all of them

which ion channels may serve as pharmacological targets for treating epilepsy? select all that apply calcium channels glutamate channels GABA receptors voltage-gated channels

all of them

many phospholipase C enzymes contain pleckstrin homology domain. what is the function of these domains? bind DNA phosphorylate proteins phosphatase proteins bind proteins bind phosphatidylinositol

bind phosphatidylinositol

What is the mechanism by which voltage-gated channels open in response to voltage changes? voltage changes cause release of ligand voltage changes shift the receptors from the inactivated to active state charged residues in the channel lead to a conformation change voltage changes lead to increased force from ions attempting to pass through voltage changes increase ion channel expression

charged residues in the channel lead to a conformation change

What is the relationship between conductance across a membrane and the number of channels that are open in that membrane? conductance is proportional to the number of receptors conductance is inversely proportional to the number of receptors conductance increases exponentially with increasing numbers of receptors conductance decrease exponentially with increasing numbers of receptors

conductance is proportional to the number of receptors

Which of the following may directly result from a spontaneous conformation change in GPCR? hydrolysis of GTP to GDP conversion of GDP to GTP receptor internalization constitutive activity

constitutive activity - in the absence of a ligand

B-arrestin has what effect on ERK signaling? increases it has no effect on it decreases it

increases it - ERK is the same thing as MAPKs - B-arrrestin - activates MAPKs (including ERK)

PI3K is an __________ protein. extracellular intramembranous intracellular

intracellular

where are the G proteins located in relation to the cellular membrane? extracellularly intramembranous intracellularly

intracellularly - the a, B, and gamma subunits are located intracellularly

If you are measuring the voltage across a cell membrane and place one electrode just outside the membrane, in which location should you place the other electrode in order the measure the greatest voltage difference? intracellularly, near the membrane intracellularly, away from the membrane extracellularly, near the membrane extracellularly, away from the membrane

intracellularly, near the membrane

the substrate of PI3K, PIP is what type of molecule? carbohydrate lipid protein nucleic acid inorganic

lipid

hyperpolarization following an action potential induced by ACh administration is primarily caused by activation of which receptor? mAChR nAChR serotonin GABA Glutamate

mAChR

which molecule/atom acts as an endogenous modulator of NMDA glutamate receptor activity? ACh Bungarotoxin Nicotine Calcium Magnesium

magnesium

does TGF-B treatment cause cells to grow more or less in soft-agar assay? more less

more - in the absence of TGF-B, cells will actually die

which statement about GPCR selectivity is correct? multiple orthosteric agonists binding the same site must produce the same effect multiple orthosteric agonists binding the same site may produce different effects allosteric modulators will have the same effect on all orthosteric agonists

multiple orthosteric agonists binding the same site may produce different effects

two neurons show the same current flow upon activation in response to the same stimulus. if neuron A has channels that stay open longer, which situation would explain how the two neurons achieve equal current? neuron A has more channels neuron B channels close sooner neuron A channels close faster neuron B channels are smaller neuron B has more channels

neuron B has more channels

Assume you have receptor antagonists that are able to stop receptor signaling immediately. For which type of receptor would it take the longest to see the effects of your drug at the cellular level? kinase-linked receptors channel-linked receptors nuclear receptors g-protein coupled receptors

nuclear receptors - takes hours already

For which type of receptor would having adequate membrane permeability of an agonist be most critical? kinase-linked receptors channel-linked receptors nuclear receptors g-protein coupled receptors

nuclear receptors - the receptors are intracellularly so the agonist has to be able to get into the cell. If not it will not work all the others requires extracellular ligands

would it be most beneficial for a large, well-developed tumor to up-regulate or down-regulate the TGF-B pathway? up-regulate down-regulate

up-regulate

Where, in relation to protein-coding regions of a gene, are the binding sites that become occupied by nuclear receptors? upstream within the coding region downstream

upstream - where transcription binds

the presence of hexamethonium will have which effect on the ACh response curve when applied to an AChR? increased maximal response decreased maximal response

decreased

what is the relationship between specific GPCRs and Ga proteins? each GPCR activates only on type of Ga proteins each GPCR activates multiple types of Ga proteins

each GPCR activates multiple types of Ga proteins

does the presence of oncogenes make it harder or easier to develop selective anti-cancer agents with fewer side effects? harder easier

easier - now we are targeting something directly to that cancer - oncogenes gives us a target

the B-arrestin mediated internalization of GPCRs occurs through which process? cytokinesis exocytosis pinocytosis endocytosis

endocytosis

where do GPCR agonists bind in relation to the cellular membrane? extracellularly intramebrously intracellularly

extracellularly

death ligands directly activate the _________ apoptotic pathway. intrinsic extrinsic

extrinsic intrinsic is wrong - it indirectly activates this

Which type of receptor most often utilizes second-messenger systems in its signaling? kinase-linked receptors channel-linked receptors nuclear receptors g-protein coupled receptors

g-protein coupled receptors - only one that utilizes second messengers

the resting membrane potential of a neuron is _______. 12 mV -90 mV 155 mV 4.2 mV 145 mV

-90 mV

Which of these caspases is an effector caspase? 2 3 8 9 10

3

which statement best explains how benzodiazepines influence the physiological response to AChR agonists? the acts as AChR antagonists they increase the affinity of AChR agonists the decrease the affinity of AChR agonists they block sodium flow through AChR receptors they increase activity of GABA receptors, blunting the effects of AChR agonists

they increase activity of GABA receptors, blunting the effects of AChR agonists

Using the Nernst equation, calculate the potential across a membrane that has a 45 mM Na+ extracellularly and 150 mM Na+ intracellularly. 58 mV -58 mV 30 mV -30 mV 0.5 mV -0.5 mV

-30 mV

to maximize the activity of an a4B2 nAChR, how many agonist binding sites should be occupied? 0 2 3 4 5

2

to maximize the activity of an a7 nAChR, how many agonist binding sites should be occupied? 0 2 4 5

2

What is the effect of one cycle of the sodium potassium pump in cells? 3 sodium ions in, 3 potassium ions out 3 sodium ions out, 3 potassium ions in 2 sodium ions in, 3 potassium ions out 2 sodium ions out, 3 potassium ions in 3 sodium ions in, 2 potassium ions out 3 sodium ions out, 2 potassium ions in

3 sodium ions out, 2 potassium ions in

using the Nernst equation, calculate the potential across a membrane that has a 45 mM Na+ intracellularly and 150 mM Na+ extracellularly. 58 mV -58 mV 30 mV -30 mV 0.5 mV -0.5 mV

30 mV

When we are developing drugs, we usually strive to achieve the best specificity that we can. However, several of the receptors you learned about affect multiple downstream events simultaneously upon activation. Why might that make it difficult to develop drugs for these pathways?

A single receptor can affect several different pathways and a single drug will affect the function of different pathways, which can lead to actions that we do not want. It is difficult to develop a drug that will only affect one or two signaling pathways because they will affect multiple different pathways and you cannot really make it just for one. If we inactivate way upstream, then we will inactivate all of the pathways but if we inactivate a little downstream we might only inactivate some pathways

Explain the role that β-arrestin plays in the ability of our eyes to adjust to light and dark conditions.

B-arrestin binds to and deactivates phosphorylated light-activated opsins to return vision to normal. Visual arrestin 1 binds to and deactivates phosphorylated light, which is critical for normal vision. So this pathway is crucial to adjusting our eyes to light and dark conditions.

For what biological reason would chemotherapy induce apoptosis? (i.e. Apoptosis is cell suicide, so why do cells exposed to chemotherapeutics commit suicide?)

Chemotherapy induces apoptosis because it wants the cancer cells to stop dividing so it will kill them. One of the possible ways that chemotherapeutic agents trigger cell death is by inducing the release of cytochrome c from mitochondria. It is vital to stop the cancer cells from dividing, therefore it is vital to induce apoptosis.

We saw that GPCRs have a basal level of constitutive activity. Not all receptors do. Why might having this constitutive activity be a benefit to the cells?

Constitutive activity is when a receptor can produce a response in the absence of a ligand. GPCRs has a wide range of activities and this is beneficial because having this constitutive activity gives GPCR the ability to undergo agonist independent isomerization from an inactive to an active state.

We saw that many drugs target GPCRs, but GPCRs are particularly difficult to target using rational drug design or computer modeling. Why might that be?

GPCRs are difficult to target using rational drug design or computer modeling because these identify selective ligands that act on a single or multiple drug targets to achieve their effect. However GPCRs are challenging because of its diversity of different conformational changes so it is tough to target specific receptors on GPCRs because of its diversity.

which G-protein subunit shows the greatest evolutionary diversity in human cells? Ga GB Gy

Ga - 20 of them

What protein is responsible for the hydrolysis of GTP and subsequent inactivation of the Ga subunit? GPCR Ga GB Gy GAP GEF

GAP - converts GAP in GDP GEF is wrong - converts GDP into GTP

Is it more likely to find G-proteins bound to a GPCR that is also bound to GTP or GDP? GTP GDP

GDP

which enzyme is responsible for inactivation Ras? AKT P85 GNEF PTEN

GNEF

the GPCR "signaling barcode" refers to signatures in what form? GPCR conformation B-arrestin conformation Ga binding GPCR phosphorylation

GPCR phosphorylation

What is the relationship between Ras and Myc mutations in cancer? they work in a synergistic fashion to increase death they work in an addictive fashion to increase death ras mutation increase the lethality of Myc inhibitors Myc mutations increase the lethality of Ras inhibitors

Myc mutations increase the lethality of Ras inhibitors

Is it more likely for a G-protein coupled receptor agonist to bind near the N- or C-terminus of the receptor? N-terminus C-terminus

N-terminus - the agonist is extracellular for GPCR so it will bind near the N-terminus

Next-generation sequencing is often touted as a game-changer in cancer diagnostics. What are two ways that it is helpful for this? You will likely have to do some research to answer this.

Next-generation sequencing offers ultra-high throughput, scalability, and speed. It is is used to determine the order of nucleotides in entire genomes or targeted regions of DNA or RNA. It allows us to identify novel and rare cancer mutations. A major advantage of these sequencing is that it can detect abnormalities across the entire genome which includes substitutions, deletions, insertions, duplications, copy number changes, and chromosome inversions/translations. It can detect all these abnormalities using less DNA than required for the traditional DNA sequence approaches. Also it is less costly and is quicker has mentioned previously. There are many advantages that make this approach a game-changer. Compared to traditional sequencing, NGS holds many advantages, such as the ability to fully sequence all types of mutations for a large number of genes (hundreds to thousands) in a single test at a relatively low cost. However, significant challenges, particularly with respect to the requirement for simpler assays, more flexible throughput, shorter turnaround time, and most importantly, easier data analysis and interpretation, will have to be overcome to translate NGS to the bedside of cancer patients. Overall, continuous dedication to apply NGS in clinical oncology practice will enable us to be one step closer to personalized medicine. Cancer is a heterogeneous disease that arises from accumulation of DNA mutations. New sequencing technologies will have a significant impact on cancer diagnosis, management, and treatment. Human genomes and thousands of cancer genomes sequenced with NGS provide a road map of the normal human genome and a landscape of mutations in cancer genomes across many cancer types. This allows us to better understand the molecular mechanism of oncogenesis and the rationale for molecule-guided therapies[11]. It will be possible in the near future to sequence both the normal and cancer genomes of every patient. Normal genome sequencing will indicate the patient's genetic background for inherited cancer risk and drug metabolism, thus enabling identification of high-risk patients and chemotherapeutic drugs with the greatest potential effectiveness and fewest potential side effects. Cancer genome sequencing can be used to monitor the disease-specific molecular genotype and guide targeted therapy design or selection.

What enzyme reverses the effects of PI3K? Ras AKT P85 GEF PTEN

PTEN

Different Smad complexes bind different genes. which group of smads is responsible for this specificity? R-smads Co-smads I-smads

R-smads - determine specificity of DNA-binding partner interaction

Why would a translocation that put Ras behind the promoter region of the actin gene lead to the formation of an oncogene?

Ras controls cell growth, proliferation, and migration of cells. Mutations in this gene could cause cell proliferation resulting in cancer cells. The actin gene is an essential gene for cell division, migration, and more in the cytoskeleton. As the Ras gene is mutated and controls cell growth, so the mutations will favor excess cell growth with the help of actin. There will be no programmed cell death due to the mutations which will lead to uncontrolled proliferation and lead to cancer cell production and therefore leads to the formation of an oncogene. Actin is the structural protein so the promoter is always on because was always need more actin. It will make more and more actin so it will help cause a proto-oncogene into a oncogene

We saw that most cancer mutations in the Ras/MAPK pathway occur upstream of MAPK rather than in MAPK itself. What might be a reason for that?

Ras/MAPK is one of the pathways in RAS. MAPK is a downstream signaling molecule that is activated by RAS. When Ras is mutated, it is highly expressed and has given MAPK to regulate the downstream signaling. This abnormal signaling will lead to uncontrolled cell proliferation and resistance to apoptosis upstream.

Which protein ultimately is translocated from the cytoplasm to the nucleus as a result of JAK signaling? JAK GRB2 SH2 PI3K STAT

STAT - it will dimerize and nuclear translocation

in the TGF-B pathway, which protein becomes activated first upon binding of a ligand? R-Smad TGFBR1 Co-Smad TGFBR2

TGFBR2 - this then phosphorylates into TGFBR1 which then phosphorylates into Smad

Signaling pathways often require receptor dimers to become active. What would be an advantage of the extrinsic apoptosis pathway requiring a trimer? I can't think of any other pathway that uses a trimer, so there must be a reason.

The advantage of using a trimer would be even more precise signaling. Receptor dimers are more precise than monomers and can bind to ligands with greater affinity than monomers so using a trimer would even have greater affinity and even more precise signaling.

What is a plausible reason the extrinsic apoptosis pathway cross-activates the intrinsic pathway, but the intrinsic pathway doesn't cross-activate the extrinsic pathway? Hint: look at the direction of flow of the signals in the figure

The extrinsic pathway can cross over because it leads to the activation of caspase. Caspases cleave the protein Bid, which is involved in the intrinsic pathway. The reason that the reverse cannot happen is because the intrinsic pathway does not cross-activate the extrinsic pathway because the proteins involved are not involved in the extrinsic pathway.

What is the fundamental difference between the inside-out and outside-out patch clamp techniques? What is an advantage of each?

The inside-out patch configuration allows the recording of single channels and bath perfusion of the cytoplasmic face of the membrane. This perfusion allows the investigation of various agents and how they can influence inactivation of the channels. An advantage of using this is that it is very stable and gives access to the surface through the bath. This method is used when changes are being made at the intracellular surface of the ion channels. The outside-out patch also allows for single channel recording. However this types has an advantage of allowing the fluid on the extracellular side of the patch to be readily changed. This type of patch allows for the studying of receptor activated ion channels.

Describe the general types of molecules that serve as ligands for the toll-like receptors.

The ligands for the toll-like receptors are heat shock proteins, glycolipids, lipopolysaccharide, fibrinogen, and more. The toll-like receptors are involved in the innate immune system and are single-pass transmembrane proteins. - signal stress, infection, damage - signs that something bad is happening and we need to activate the innate immune system

You are developing a TGF-β agonist, but you don't yet know which specific proteins it is signaling through. You want to do a single Western blot to measure changes in signaling activity, regardless of which pathway is being activated. For which protein involved in these pathways could you measure the levels in the nucleus of cells and be confident in your results? Why?

The protein that could be measured is the bone morphogenetic protein (BMP), which is involved in the TGF pathway. This protein can be measured because a change in the level of this protein will show an increase or decrease in the TGF pathway. You want to use one western blot. You want to look for the Smad 4. If you see Smad 4 in the nucleus then you know that TGF-B signaling is activated

We saw that signaling based on channel-linked receptors is the fastest signaling mechanism. Why is this faster than other mechanisms?

The reason that inotropic receptors are the fastest is that they open quickly and do not have to activate multiple molecules in the intracellular mechanism. They are quick opening and only remain open for a very short time. The second fastest signaling mechanism is the metabotropic - GPCR, which takes longer than channel-linked receptors because it has to activate multiple molecules intracellularly. the only thing that happens here is - ligand binds, receptor opens and ions flow in all the others have to use proteins and

GPCRs are also known as 7-trans membrane receptors (7-TMRs). What is a plausible explanation as to why they have exactly 7 transmembrane domains rather than a different number?

The reason that it is called 7-TMRs is that it spans the membrane 7 times. It has an extracellular N-terminus with 7 TMRs, which is connected by 3 intracellular and 3 extracellular loops. Also has a C-terminus. It has always spanned the membrane 7 times, which is where it gets its name.

You've discovered a new gene, G8R. Describe two experiments you could do to determine whether it is a proto-oncogene. Explain the experimental set-up as well as how you would interpret the results.

There are many experiments that one could use to determine whether a new gene is a proto-oncogene. There is in-vivo experiments and there are also in vitro evidence. An in vivo experiment would include putting that new discovered gene in a nontumorigenic cell line and see if it has the ability to develop tumors. Also an in vitro experiment would be to cause focus formation which would be the loss of contact inhibition. If the cells can continue to grow even after they run into each other then it would be cancerous - the cells can pile up on each other so continued proliferation.

There have been many attempts to block TGF-β signaling in cancer through many different mechanisms, but none of been very successful. Why do you think this is?

There have been some successful preclinical studies in mouse models but have not been approved. There are many reasons but TGF-B has a critical role in maintaining tissue homeostasis and has a role as a tumor suppressor. These are two big reasons that treatment blocking TGF-B signaling has not been very successful because of its side effects. Most likely that TGF-B signaling has many different pathways. It is not absolutely necessary for tumor survival but it helps with its survival.

The EGFR kinase activity independent transactivation of the Ras pathway does require EGFR. Explain this apparent contradiction.

There is a contradiction because the mechanisms by which different receptors transactivate EGFR are distinct depending on their ligand targeting and kinetics and more. The transactivation by IGF-1 acts through its own receptor but still has the same end result because there is still integration from different receptors by the EGFR.

We have kinases that phosphorylate tyrosine, serine, and threonine. What do these three amino acids have in common that makes them targets of kinases?

These 3 amino acids all contain a hydroxyl group, which allows kinases to act on them by removing a phosphate group of ATP and attaching it to the free hydroxy group.

Which of the following drugs would have no effect on the spontaneous conformation changes seen in GPCRs? full agonist partial agonist inverse agonist antagonist

antagonist - no effect on conformation changes, it just blocks the agonist from binding agonist is wrong - activates it inverse agonist is wrong - converts it from active to inactive form

The levels of which second-messenger would be expected to increase following administration of nitroglycerin? Ca2+ cAMP carbon monoxide diacylglycerol cGMP Kaboom!

cGMP - the most common protein target for NO (nitroglycerin) is soluble guanylyl cyclase, an enzyme that generates the second messenger cGMP. - the signaling functions of NO begin with its binding to protein receptors on or in the cell. The binding sites can be either: a metal ion in the protein or one of its S atoms (e.g., on cysteine).

PLC exerts some of its effects through the modulation of which physiological ion? sodium potassium calcium chloride

calcium

which apoptosome component is responsible for directly activating the effector caspases? APAF-1 Cytochrome C Caspase 9

caspase 9 - attached to the apoptosome and is part of it and activates the effector caspases - located intracellularly

would it be most beneficial for an early tumor to up-regulate or down-regulate the TGF-B pathway? up-regulate down-regulate

down-regulate - before cells are cancer cells, TGF-B acts primarily as a growth inhibitor so tumor cells do not want to inhibit its in growth

Which form(s) of oncogene activation involve(s) a mechanism that will NEVER directly change the DNA sequence in a cell. mutation amplification rearrangement promoter insertion hypomethylation

hypomethylation - changes the state of the DNA and how actively its being transcribed. Does not change the sequence - mutation is wrong - because it mutates the DNA - amplification is wrong - inserting new DNA into chromosomes - rearrangment is wrong - means taking the DNA and rearranging it - promoter insertion is wrong - inserting new DNA

How is the activity of the IKK complex modulated in order to determine whether the complex feeds into the canonical or non-canonical signaling pathway? if the complex includes NEMO it feeds into the canonical pathway. if the complex includes DORY, it feeds into the non-canonical pathway. if the complex includes phosphorylated IKKB it feeds into the canonical pathway. if the complex includes phosphorylated IKKa, it feeds into the non-canonical pathway. if the complex is cystolic it feeds into the canonical pathway. if the complex is in the nucleus, it feeds into the non-canonical pathway. if the complex is completely degraded by the proteasome it feeds into the canonical pathway. if the complex is partially degraded by the proteasome, it feeds into the non-canonical pathway.

if the complex includes phosphorylated IKKB it feeds into the canonical pathway. if the complex includes phosphorylated IKKa, it feeds into the non-canonical pathway. - if the complex contains Ikk-B that is phosphorylated, it activates the canonical pathway -> phosphorylates IK-B - if the complex contain IKK-A that is phosphorylated, it activates the non-canonical pathway -> phosphorylates Ik-A

based on the effects of Nf-kB signaling, would cancer cells be expected to increase or decrease its activity for their own benefit? increase decrease

increase

Overexpression of the BAK protein would be expected to _______ the rate of apoptosis. increase decrease

increase - BAK protein is part of the Bcl-2 proteins, which occurs in the intrinsic pathway

which statement best describes the role of the MyD88 protein in Nf-kB signaling? it phosphorylates NF-kB it directly degrades IkB it prevents the premature activation of NF-kB its acts as a scaffold to recruit the IKK complex it acts as a transcription factor in the nucleus

it acts as a scaffold to recruit the IKK complex - MyD88 binds to the receptors and then the IKK complex. It does not actually do anything so therefore it recruits the complex to the receptor

Which statement best describes the role of p50 protein in NF-kB signaling? it phosphorylates NF-kB it directly degrades IkB it prevents the premature activation of NF-kB its acts as a scaffold to recruit the IKK complex it acts as a transcription factor in the nucleus

it acts as a transcription factor in the nucleus - one of the subunits of the Nf-kB complex

What is the primary effect on the signaling from activated GPCRs due to the activation of PKA by cAMP? it stops the signaling its spreads the signal from one cell to the other it allows the signal to move into the nucleus

it allows the signal to move into the nucleus

Which statement best describes the role of the IKK protein in NF-kB signaling? it phosphorylates NF-kB it directly degrades IkB it prevents the premature activation of NF-kB its acts as a scaffold to recruit the IKK complex it acts as a transcription factor in the nucleus

it phosphorylates NF-kB - this occurs in the canonical pathway in the non-canonical pathway, it phosphorylates p100 (Nf-Kb)

Which statement best describes the role of IkB protein in NF-kB signaling? it phosphorylates NF-kB it directly degrades IkB it prevents the premature activation of NF-kB its acts as a scaffold to recruit the IKK complex it acts as a transcription factor in the nucleus

it prevent the premature activation of NF-kB

A GRK inhibitor would have what effect on GPCR inactivation in the presence of a GPCR agonist? it would decrease it it would maintain the same rate of inactivation it would increase it

it would decrease it - you would cause GPCR desensitization which would defcrease it

Which domains are found in all class I, II, and III PI3Ks? select all that apply? kinase domain ras-binding domain C2 domain helical domain PX domain

kinase domain C2 domain helical domain

observation of which of the following would be an indication of ongoing apoptosis? inflammation lysis overactive lysosomes membrane blebbing

membrane blebbing

through which mechanism is glutamate signaling stopped? reuptake of glutamate metabolism of glutamate

re-uptake