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Biochem block 3 > Lecture 1b-cell signaling > Flashcards

Lecture 1b-cell signaling Flashcards

1
Q

What is the def of cell signaling

A

cell communication involvies release of substance (e.g. hormones, ligands) from a cell, dection by target cell and conversion of signal to a biological outcome

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2
Q

What are the 3 steps of cell signaling

A
  • Reception: target cell senses the substance in its exogenous environment/ intercellular signaling-contact dependent or contact independent
  • Transduction: conversion of the signal via a cascade of molecular events /intracellular signaling
  • Response: specific cellular effect attributed to the signaling molecule/E.g: transcription of genes resulting in protein expression mediating a biological response
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3
Q

What are intracellular consquences of hormone receptor interaction

A
  • hormone gated ion channels can change membrane potential
  • A receptor enzyme is activated by an extracellular hormone
  • a 2nd messenger generated inside the cell acts as a allosteric regulator of one of more enzymes
  • a steroid or steroid-like molecule changes a the level of gene expression evia nuclear hormone receptor proteins
  • a receptor recruits a soluble protein kinase from the cytosol to trigger a signaling cascade
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4
Q

What are the modes of intercelluar signaling for reception

A

Contact dependent: Juxtacrine
Contact independent: endocrine, synaptic, autocrine and paracrine

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5
Q

Contact dependent

A

juxtacrine

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6
Q

contact independent

A
  • Endocrine: sender cell release hormone to go into blood
  • Synaptic: with neurotransmitters off sender neuron, synapse and target cells
  • Autocrine: taget receptors on the same cell
  • Paracrine: sender cell sends local medaitor to target cells
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7
Q

What is transduction

A

hormones transduce effects through cellular signaling

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8
Q

Tissues capable of responding to hormones have 2 properties in commone:

A
  • They posses a receptor having very high affinity for hormone
  • The receptor is coupled to a process that regulates metabolism of the target cells
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9
Q

What are the secreted molecules

A
  • Hormones: peptide and steroid hormones
  • neurotransmitters
  • Peptides
  • lipids
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10
Q

What are the receptors for secreted molecules

A

Intracellular receptors
* Steroid hormones
* Estrogens
* Androgen

Cell surface receptors
* Peptide hormones
* Growth factors

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11
Q

Are intracellar receptors hydrophobic or hydrophillic

A

Hydrophobic

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12
Q

Are cell surface receptors hydrophobic or hydrophillic

A

hydrophillic

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13
Q

Explain the process of the glucocorticoid receptors and estrogen receptor

A
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14
Q

Where is the glucocorticoid receptor found?

A

cytosol then translocates into the nucleus to activate transcription of a gene

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15
Q

Where is the estrogen receptor located?

A

Nucleus

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16
Q

What are the two types of steroid hormone receptor activities

A
  • Genomic action: slow (minutes)
  • Nongenomic action: Rapid (seconds)
17
Q

What are the major subtypes of estrogen and what is it synthezied from?

A
  • ERalpha and ERbeta
  • from cholesterol
18
Q

What is the difference of the subtype of estrogen?

A

The A/B region (ligand independent activation function domain) is larger in the ERalpha

19
Q

ERa and ERb exert differential effects on what?

A

growth and differentiation in tissues, including bone, colon, uterus, liver, brain, and mammary gland

20
Q

What is the therapeutic application of estrogen?

A

Selective estrogen receptor modulators (SERM)

21
Q

What is SERM

A

Selective estrogen receptor modulators
* ER ligands (synthetic)
* Exhibit ER aganistic or antagonistic activity depending on the tissue
* Induce structural changes–>affect ability to interact with cofactors–>different effects gene expression

22
Q

What is the molecular basis of SERM (ongoing research)

A
  • Receptor sub-type specificity (ERa and ERb)
  • Cell type specific co-activators and regulators
  • Cell type specific targets
23
Q

What is tamoxifen

A

competitive inhibitor of estrogen receptor (aka: SERM)

24
Q

More facts you need to know about SERM

A
  • ER subtypes are diffrentially expressed in target tissues and can be heterogeneously expressed in a particular tissue
  • SERMs have differential affinity for ER subtypes (ERa and ERb)
  • SERM binding induces specific conformational changes in ER that inflyence dimerization and binding to varuous co-factors that can determine resultant target gene activation or repression
  • 1St STERM used in clinic: Tamoxifen use in ERa positive breat cancer
25
Q

Explain the picutre of Tamoxifen

A
26
Q

In breast tissue, what is the receptor type

A

antagonist

27
Q

In uterine tissue, what is the receptor type

A

agonist: no conformationion change

28
Q

What does tamoxifen do in breast tissue

A
  • no breast cell proliferation
  • decreased cancer risk

Biochem block 3 (6 decks)

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