Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Patient Presentation > Cell Signaling > Flashcards

Cell Signaling Flashcards

1
Q

Mechanism of endocrine hormone signaling

A

Hormones are released into the bloodstream to act on target cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Mechanism of paracrine hormone signaling

A

Hormones act on adjacent cells. Do not enter the bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Mechanism of autocrine hormone signaling

A

Cell secretes the hormone and the hormone acts on the cell that secreted it (the hormone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What classes of hormones are hydrophilic and what structural characteristics of the hormone make them hydrophilic?

A

Peptides-certain amino acids are hydrophilic
Some amines-in this case catecholamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What classes of hormones are hydrophobic and what characteristics of their structure make them hydrophobic?

A

Steroids: steroids derived from cholesterol, a multi carbon ring structure
Some amines- thyroid hormones in this case

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What steroid hormones does cholesterol serve as a precursor for? What intermediate is formed before the hormones can be formed

A

Precursor: cholesterol
Intermediate: pregnenolone
Hormone products: Aldosterone,
Testosterone –> Estradiol
Cortisol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What amino acid serves as the precursor for key catecholamine hormones?

A

Tyrosine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the key amine hormones? What are they synthesized from?

A

Synthesized from tyrosine
Key amine hormones: dopamine, norepinephrine, epinephrine, thyroxine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What mechanism do peptides and catecholamines use to travel to target cell?

A

Peptides and catecholamines are hydrophilic and therefore water soluble so they can dissolve in aqueous mediums such as blood and interstitial fluid and travel and bind to extracellular receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What mechanism do steroid and thyroid hormones use to travel to target cell?

A

Steroid and thyroid hormones are not water soluble therefore they must attach to a water-soluble carrier protein. (Examples: thyroxine-binding globulin, transcortin [cortisol] , albumin [aldosterone] )

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the purpose of second messengers? What type of hormones must use secondary messengers and why?

A

Purpose of secondary messengers is to initiate signal transduction pathway that carries out the function of the hormone and alters gene expression

Hydrophilic hormones must use secondary messengers because unlike lipophilic hormones, hydrophilic hormones cannot freely diffuse across the cell membrane (bc of their polarity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Catecholamine second messenger system?

A

cAMP (Gs/Gi pathway)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Antidiuretic hormone (ADH) associated second messenger system?

A

BOTH
cAMP (Gs/Gi pathway) and IP3 (Gq pathway).
Has proteins that can bind to V1 and V2 receptors which stimulate different pathways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Follicle-stimulating hormone (FSH) associated second messenger

A

cAMP (Gs/Gi pathway)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Luteinizing hormone (LH) associated second messenger

A

cAMP (Gs/Gi pathway)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Adrenocorticotropic hormone (ACTH) associated second messenger

A

cAMP (Gs/Gi pathway)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Thyrotropin-releasing hormone associated second messenger

A

IP3 (Gq pathway)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Angiotensin II associated second messenger

A

IP3 (Gq pathway)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What characteristic of the G protein-coupled receptor accounts for the variation in second messenger pathways?

A

GPCR comprised of G protein. The G protein has 4 main subtypes (3 from alpha subunit and 1 from beta-gamma subunit):
Gs (G stimulatory cAMP)
Gi (G inhibitory cAMP)
Gq (IP3/DAG)
Beta-gamma pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the effect of lipophilic hormones binding to intracellular receptors

A

They bind to a target gene and directly repress or enhance transcription of the gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Process that allows cells to adjust their sensitivity to a hormone

A

Adaptation: specifically upregulation or downregulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe what permissive effect of a hormone means

A

Permissive effects means that a hormone/molecule is required for another hormone to act at its full capacity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe what is meant by synergistic effect of a hormone

A

Negative or positive additive effects of hormone. Summation of both hormones. Great example is FSH and estrogen in ovaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How does humoral stimulus regulate hormone release?

A

Humoral stimulus is a change in the body composition that leads to hormone release. Ex: change in serum ion concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Difference between antagonistic effect and negative synergistic effect

A

Antagonist effect: hormones always have opposing effects
Negative synergistic effect: this hormone works to decrease effect of another hormone. Not set up within body to be the counterpart of another hormone

26
Q

How does hormonal control regulate hormone release?

A

A released hormone causes the release of another hormone. Hormones act on target cell to release another hormone

27
Q

How does neural stimulation regulate hormone release?

A

Neural sign stimulates release of hormone. Ex: PNS stimulated by vagus nerve to release gastrin when resting and digesting

28
Q

Key examples of peptide hormones

A

Insulin, glucagon, prolactin

29
Q

Peptides synthesized from what

A

Synthesized as prohormones and must be further processed to activate as peptide

30
Q

Agonist v antagonist ligand functions

A

Agonist: ACTIVATES receptor through conformation change
Antagonist: INHIBITS activation of receptor by blocking receptor binding site without being able to change conformation of receptor therefore without activating receptor

31
Q

Five principles of receptor-ligand actions

A
  1. Specificity
  2. Amplification: multiple secondary messengers can be activated
  3. Desensitization via processes such as structural changes and endocytic vesicle/acidification/dissociation
  4. Modularity: parts of signal transduction pathway broken into compartmentalized paths
  5. Integration: signaling pathways regulated by activation of multiple receptors
32
Q

Difference and examples of:
Primary/first messenger
Primary effector
Secondary messenger
Secondary effector

A

Primary messenger: ligands that bind to extracellular receptor (ex: hormone, neurotransmitter)
Primary effector: extracellular receptor on cell surface that transfers signal transduction process to inside of cell
Secondary messenger: intracellular molecules that bind to secondary effector (ex: cAMP)
Secondary effector: intracellular receptors that trigger changes (ex: protein kinase A, PKA)

33
Q

Describe the mechanism pathway for the activation of the trimeric G protein-coupled receptors (GPCR) when the G-alpha s subunit is activated

A
  1. Hormone binds to GPCR inducing conformational change of hormone
  2. Gα subunit of the G protein exchanges the GDP its bound to for GTP making Gα+GTP active
  3. Gα+GTP dissociates from trimer leaving beta-gamma
  4. Gα+GTP activates adenylyl cyclase
  5. Activation of adenylyl cyclase stimulates conversion of ATP –> cAMP
  6. cAMP goes to activate protein kinase A (PKA) and PKA goes to effect target cells
34
Q

How does the association and disassociation of GPCR and Gα regulate the cAMP pathway?

A

Association of complex leaves it in its trimeric inactive form (no adenylyl cyclase activation)
Dissociation of complex allows for the GDP to be phosphorylated and converted into GTP to activate the subunit (adenylyl cyclase activation)

35
Q

What is an example of an antagonist effect within the GPCR pathway? How are the effects antagonistic?

A

The inhibitory and stimulatory Gα subunits of the trimeric G protein. The stimulatory Gα activates cAMP and the inhibitory Gα inhibits cAMP production

36
Q

Describe the pathway for a ligand that is bound to a GPCR G protein with a G alpha q subtype

A

Phosphoinositol system (IP3/DAG)
1. GPCR is activated by ligand binding
2. Phospholipase C is activated as a result of GPCR activation
3. The phospholipase C enzyme cleaves the C 4,5-BP to form inositol triphosphate (IP3) and diacylglycerol (DAG) (secondary messengers)
4a. IP3 stimulates release of intracellular calcium that goes on to act on muscle cells and liver cells
4b. DAG activates protein kinase C (PKC) which binds Ca++ and phosphatidylserine to activate downstream effects

37
Q

What characteristic do tyrosine kinases, calcium/calmodulin, and guanylate cyclase pathways all have in common?

A

They’re all monomeric G-protein pathways

38
Q

Receptor tyrosine kinase (RTK) function, mechanism of action, and important examples of G proteins

A

Function: role in GROWTH FACTORS (think about mutation –> cancer), hormones, cytokines

Mechanism:
1. Receptor activation causes dimerization and autophosphorylation
2. Activation of monomeric G proteins –> activation of additional G proteins –> activation of TRANSCRIPTION FACTORS

Classic examples of small G proteins: Ras, Raf, Rho

39
Q

Calmodulin mediates which processes? What event must occur for calmodulin to be active?

A

Activated via calcium entrance into cell and subsequent binding to calmodulin
Mediates: inflammation, metabolism, apoptosis, muscle contraction

40
Q

A signaling pathway activated phospholipase C. What is the secondary ionic molecule that is probably released in this pathway?

A

Ca2+, release triggered by activation of IP3

41
Q

What type of receptor does GABA and other neurotransmitters use?

A

Ligand-gated ion channels

42
Q

What is the function of cell surface adhesion receptors? What are the principle families of these receptors?

A

Play a role in cell signaling pathway. Can work through secondary messengers or a direct signal. Mediate cell adhesion by binding to the surface of an adjacent cell or the extracellular matrix
Principle families: integrins, selectins, and cadherins

43
Q

Nuclear receptor function and domains? Classic example of molecule?

A

Function: receptors INSIDE cell, purpose to bind to nuclear DNA and act as transcription factor

3 domains:
Transcriptional domain
DNA binding domain
Ligand binding domain

Classic example of nuclear receptor: PARR

44
Q

Describe the mechanism pathway for the activation of the trimeric G protein-coupled receptors (GPCR) when the βϒ subunit

A
  1. βϒ activates phospholipase A2
  2. Phospholipase A2 activates arachidonic acid
  3. Arachidonic acid activates 3 different pathways
45
Q

General mechanism of catalytic receptors? Examples of catalytic receptors?

A

When the hormone binds to the receptor, the receptor itself gains enzymatic activity to initiate second messenger cascade system

46
Q

Describe the mechanism/pathway of tyrosine kinase receptors. What is the classic example of a tyrosine kinase receptor?

A

Classic example: insulin

  1. Hormone binds to receptor
  2. Receptor dimerizes and begins to autophosphorylate (from tyrosine residues)
  3. Presence of phosphorylated regions of receptor activates second messenger system that recruits small G proteins (ras, raf, rho)
  4. Small G proteins cause activation of transcription factors
  5. Activation of MAPK and Ras pathways
47
Q

What is the general mechanism of guanylate cyclase?

A

Parallel of its other purine cyclase: adenylyl cyclase just with guanylate instead

  1. Ligand binds and activates guanylate cyclase
  2. Guanylate cyclase converts GMP to cGMP
  3. cGMP activates protein kinase G
  4. protein kinase G acts as intracellular secondary effector

Primary effector for nitric oxide

48
Q

What hormone does production of cortisol rely on?

A

Adrenocorticotropic hormone (ACTH)

49
Q

Rate limiting steps and enzymes in steroid production?

A

Step: cholesterol being transferred from cytosol to mitochondria
Enzyme: steroidogenic acute regulatory protein (StAR)

Step: cholesterol –> pregnenolone
Enzyme: desmolase

50
Q

How does adrenocorticotropic hormone (ACTH) stimulate the production of cortisol?

A

ACTH stimulates the production of StAR (the enzyme that moves cholesterol into the mitochondria for continued synthesis)

ACTH also upregulates the activity of cholesterol desmolase (the enzyme that converts cholesterol to pregnenolone and furthers the synthesis of cortisol)

51
Q

What mechanism is needed for cortisol to diffuse through adrenal cell membranes? What mechanism is needed for cortisol to diffuse through the blood stream?

A

Cortisol is a steroid, therefore its lipophilic. Cortisol can freely pass through the cell membrane

Cortisol needs a corticosteroid-binding globulin (CBG) (also called transcortin) to travel through the bloodstream. This CBG is needed for the same reason that cortisol travels through the membrane freely, its lipophilic in an aqueous solution therefore it needs a carrier protein.

52
Q

What is the name of the cortisol cell receptor? Where is the receptor located?

A

Cortisol binds to the glucocorticoid receptors (GRs)
Receptor is located in the cytosol, inside the cell because cortisol is lipophilic and can freely cross the plasma membrane

53
Q

How does cortisol increase serum glucose concentration via the liver?

A

Increases gluconeogenesis
Decreases glycogen formation

54
Q

What effect does cortisol have on the immune system? Specifically on wound healing and immunity?

A

Wound healing: decreased
Immunity: decreased

For cortisol to work as an anti-inflammatory it must decrease inflammation and immune responses, therefore decreasing wound healing and overall immunity. Specifically it decreases inflammation by inhibiting production of proinflammatory mediators such as leukotrienes, prostaglandins, etc.

55
Q

What three organs are involved in cortisol synthesis

A

Hypothalamus, pituitary gland, and adrenal glands which form the HYPOTHALAMIC-PITUITARY-ADRENAL AXIS (HPA)

56
Q

What is the function of the HPA

A

Hypothalamic-pituitary-adrenal axis (HPA) acts as a hormone modulating center

57
Q

What are the steps that occur for cortisol to be synthesized?

A
  1. hypothalamus releases CRH (corticotropin-releasing hormone) to activate anterior pituitary
  2. Anterior pituitary releases ACTH
  3. Release of ACTH triggers cortisol synthesis
58
Q

What two tissues (that we need to know) does epinephrine act on? What metabolic effects occur as a result?

A
  1. Liver cells: acts to increase blood glucose
    Increases glycogen breakdown
    Increases gluconeogenesis
  2. Muscle cells: acts to increase ATP
    Increases glycogen breakdown
    Increases glycolysis
    Increases beta oxidation
59
Q
  1. What are the target proteins of epinephrine?
  2. How does epinephrine change the structure of its target proteins?
  3. How are these target proteins affected by epinephrine’s signaling cascade?
A
  1. glycogen synthase, phosphorylase kinase, glycogen phosphorylase
  2. each target protein is phosphorylated by Protein Kinase A (PKA)
  3. glycogen synthase - inhibited (enzyme responsible for making glycogen)
    phosphorylase kinase - stimulated (enzyme responsible for adding phosphate to glycogen phosphorylase)
    glycogen phosphorylase - stimulated (enzyme responsible for glycogen degradation –> glucose)
60
Q

How is cyclic AMPs/GMPs broken down into their non-cyclic versions?

A

Phosphodiesterase (PDE)

61
Q

What is the role of protein phosphatases?

A

For epinephrine specifically, the protein phosphatases remove phosphates from TARGET proteins such as glycogen synthase, glycogen phosphorylase, to reverse stimulation/inhibition.

62
Q

Steps of cytokine induced autocrine/paracrine signaling

A
  1. Cytokine binds receptor
  2. Conformational changes occur to receptor as a result and activation of enzymes (kinases/ubiquitin-ligases/proteases) occurs
  3. Enzymes activate transcription factors
  4. Transcription factors travel to nucleus, bind to DNA, and promote transcription of genes responsible for the immune response

Patient Presentation (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions