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Cell Signaling > Cell > Flashcards

Cell Flashcards

1
Q

Name the 5 different ways cells can signal.

A

Intra-,Auto-, Juxta-, Para-, Endo-crine

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2
Q

Name the 3 categories of cell junctions.

A

Communicating, occluding, anchoring

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3
Q

Name the 6 types of junctions

A

Gap, Tight, Adherens, desmosome, Focal adhesion, Hemidesmosome

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4
Q

Gap junction proteins and their functions are :

A

Connexinx, transport cAMP, Ca and other smaller then a 1000 dalton molecules.

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5
Q

Tight junction protiens and their function

A

Occludin, claudin, form cell cell junctions by binding actin.separate epidermal layers from ECM and decide spacial polarity’of the cell

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6
Q

Adherens junctions protein and their functions

A

Cadherin that binds to actin and forms cell-cell junctions

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7
Q

Desmosomes protein and function

A

Cadherin that binds intermediate filaments and create cell-cell junctions

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8
Q

Focal adhesion protein and function

A

Integrin that binds actin in cell and fibronectin in ECM to form Cell -matrix junction

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9
Q

Hemidesmosomes, protein and function

A

Integrin protein that forms cell-matrix junction by binding keratin in cells and laminin in ECM

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10
Q

What are the two main classes of hormones give examples

A

Peptide and amino acid derived hormones (dopamine, NE,Insulin, IGF1, GH ) and Steroid hormones (Testosterone, progesterone, cortisol, aldosterone)

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11
Q

What is the main difference between. Steroid and Peptide derived hormones?

A

Peptide hormones need cell surface receptors to mediate their actions (RTKs or GPCRs) while steroid hormones can pass plasma membrane and act on cytosolic or nuclear receptors.

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12
Q

Name 3 gasotransmitters and their effects

A

NO(vasodilator by smooth muscle relaxation, inhibitor of platelet adhesion), CO(vasodilator by smooth muscle relaxation, anti-inflammatory, anti-proliferative, anti-apoptotic), H2S

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13
Q

Explain constitutive secretion

A

Vesicles constantly undergoing exocytosis (for proteins without a destination)

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14
Q

Name all the routes of protein secretion

A

Constitutive, Regulated, Transcytosis, Multivesicular transport, Microvesicles,
Shedding

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15
Q

Explain regulated secretion

A

Loaded vesicles are stored in cytosol until release signal is received

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16
Q

Explain secretory lysosomes

A

Capturing proteins and secreting them

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17
Q

Explain multivesicular transport

A

One large multivesicular body contains exosomes and release them

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18
Q

Explain microvesicles

A

Vesicles that are not from the Golgi

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19
Q

Explain shedding

A

ICD of transmembrane protein gets cleaved thus release of ECD of the protein

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20
Q

What is anterogade and retrogade transport? Name coating proteins involved

A

Anterogade : ER to cis-Golgi (COPII). Retrogade : cis-Golgi-ER (COPI)

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21
Q

What is the function of Clatherin?

A

Transports cesicles from plasma membrane to the Golgi and the from Golgi to the lysosome

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22
Q

Name the 3 steps and the a short description to each in cesicle formation

A

Cargo selection (coat and adaptor proteins accumulate, filtration by receptor), Vesicle budding( fission, GTP dependent, uncoating), Vesicle targeting and fusion (Rab-GTP)

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23
Q

Name the receptor and downstream effects of NO and CO

A

Guanyl cyclase receptor —> cGMP—> vasodilation

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24
Q

Explain the pathway for NO synthesis

A

Ach binds receptor on endothelial cell —> IP3–> Ca—> Triggers NOS

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25
Q

What do PKRs do?

A

Cytosolic proteins that dimerize and, bind to viral dsRNA and phosphorylate elF2alpha
to halt translation

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26
Q

Why mRNAs do not bind PKRs?

A

Because they are sigle stranded and too long

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27
Q

Name the steps of miRNA formation.

A

Transcription —> pri-miRNA—>Drosha4 &Pasha/DGCR8—>pre-miRNA—>Dicer—> ds-miRNA no loop—>RISC & Ago—> ss-miRNA binds to UTR on mRNA and Ago breaks down mRNA.

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28
Q

Function of siRNAs

A

In nucleus bind to promoter region. In cytoplasm perfect binding to mRNA promotes its cleavage.

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29
Q

Name the steps of Ras pathway

A

RTK-Ras-Raf-Mek-Urk

30
Q

Name general MAPK pathway downstream to RTK

A

MAPKKK—>MAPKK—>MAPK—>effect

31
Q

What are scaffold proteins used for in cell signalling?

A

To hold downstream proteins and signalling molecules close to one another, also in proper order.

32
Q

What type of receptors can activate PI3K pathway?

A

RTKs and GPCRs

33
Q

What does PI3K act on?

A

converts PIP2 to PIP3 with the help of PTEN

34
Q

Name 2 downstream effects of PI3K

A

Ras and AKT

35
Q

Name two downstream targets of PIP3

A

PDK1 and AKT

36
Q

Name a common downstream target of GPCRs and RTKs

A

Phospholipase C (PLC)

37
Q

What two compounds are needed for the activation of PKC

A

Diacylglycerol and Ca

38
Q

Name the 3 main classes of Nuclear receptors

A

Steriod receptors, Adopted Orphan receptors, Orphan receptors,

39
Q

Name the subgroups of Orphan receptors

A

Monomeric and homodimeric

40
Q

How many classifications of nuclear receptors exist(NR)?

A

NR 0-6

41
Q

What do A & B domains of nuclear receptors contain? What is the function? Where is this domain located?

A

First two transactivation domain, AF-1, N-terminal

42
Q

What does C domain of NRs contains?

A

DBD consisting of two zinc finger DNA binding motifs

43
Q

What does D domain of NRs consist of?

A

Hinge region, Nuclear localization sequence (NLS)

44
Q

What does E domain of NRs contain? Wheere is it located?

A

Ligand-binding domain(LBD) and second transactivation domain AF-2, located at c-terminal

45
Q

Sumarize the key feature of nuclear receptors

A

Ability to regulate different sets of genes within different cell types based on the tissue specific transcriptional complexes

46
Q

To what NRs can thank their key features

A

NRs function as inducible scaffolds capable of coordinating large transcriptional complexes

47
Q

Name general ligands of AhR

A

Xenobiotics, Flavonoids, Molecules formed by endogenous metabolism

48
Q

What is inactive cytosolic AhR bound to?

A

HSP90, p23 and XAP -molecule 2

49
Q

Explain main steps of the genomic activation pathway of AhR.

A

Heterodimer formation with ARNT—> BInding to Xenobiotic responsive elements (XRE)

50
Q

Name the steps of nongenomic AhR activation.

A

AhR active —> Increased Ca—> activates PKC—>phosphorylation of serine residue on Src—>ahesion disturbance, inflammation, MAPKs

51
Q

What is the function of Cytochrome P450 genes

A

Detoxification of lipophilic and nonpolar substances

52
Q

Chemicals that are able to interact with hormone producing organs or act as a hormones are called :

A

Endocrine disruptors (EDCs)

53
Q

What are dioxins?

A

Polyhalogenated aromatic hydrocarbons

54
Q

Name the steps of xenobiotic detoxification

A

Functionalization (addition of oxygen), Conjugation(adding water soluable group), Secretion(into urine or bile)

55
Q

Name the type of water soluble groups that can be added during Conjugation step

A

Glucoronic acid, Amino acid, Acetyl group, Methyl group

56
Q

What is a common intermediate product in detoxification process? Why this compound can be a problem?

A

Benzo(a)pyrene that can diffuse to the nucleus and cause DNA damage

57
Q

what are the domains of mTOR?

A

Heat repeats,FAT domain, FRB domain, Kinase domain, FATC domain

58
Q

In general what is positevely regulated by mTOR?

A

Anabolic processes, transcriptio, translation, ribosome biogenesis, nutrient transport and mitochondrial metabolism

59
Q

In general what are negatively regulated processes by mTOR?

A

Catabolic processes like mRNA degradation, ubiquitin dependent proteolysis, autophagy and apoptosis

60
Q

Name pathways that activate the mTORC1

A

Wnt(TSC2 inhibition), IGF1 and GFs via AKT mediated inhibition of TSC2, Ras via Erk that inhibits TSC2

61
Q

Name a pathway that inhibits mTORC1

A

TNF-alpha that inhibits TSC1

62
Q

What amino acids induce mTORC1 by activating GATOR2? What upstream signal they interfere with?

A

Leucin inhibits Sestrin2 and Arginine inhibits CASTOR1, both of those inhibit GATOR2

63
Q

What hypoxia, DNA-damage and glucose deprivation can lead to with regard to mTORC1

A

All lead to TSC2 activation and thus mTORC1 inhibition

64
Q

What is the main downstream effector of mTORC1

A

P70S6 kinase(S6K1)

65
Q

Give the Fenton reaction below

A

Fe(II) + H2O2 —> Fe(II) = OH(-) + °OH

66
Q

Downstream general effects of S6K1

A

Cap dependent translocation, enhanced translation efficacy, cholesterol and fatty acid synthesis, autophagy supression, oxidative pentose pathway enhance,

67
Q

Name exact downstream targets of S6K1

A

elF4B(elF4A release), SKAR(translation eficacy) Lipin (SREBP inhibitor) inhibition, ATF-4 (ribosome biogenesis), ULK1 activation (autophagy supression), TFEB inhibition (UPS turn off)

68
Q

How does mTORC2 effect IGF1 signaling?

A

Negatively, its a negative feedback loop

69
Q

What downstream phosphorylative activation effects does mTORC2 has?

A

PKA, PKC, PKG and AKT

70
Q

How does mTORC1 and S6K1 play a role in type 2 diabetes

A

Prolonged mTORC1 activation —> active S6K1 —> inactive IRS1—> no glucose transporters —> high blood sugar and hypertension

71
Q

Recite Shh pathway

A

Shh-Patched-Smoothened-Gli to GliAct activation and Gli to GliRep inhibition. GliAct transcribes Shh target genes

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