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IMS topic 6 - Endocrinology > Nuclear hormone receptors > Flashcards

Nuclear hormone receptors Flashcards

1
Q

What are steroid hormones and vitamin D derived from?

A

Cholesterol

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2
Q

What are thyroid hormones and aromatic amines derived from?

A

Amino acids e.g. thyroxine

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3
Q

What are prostaglandins derived from?

A

Fatty acids

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4
Q

Where do peptide hormones and catecholamines bind to?

A

Bind to cell surface receptors

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5
Q

Where do steroid and thyroid hormones bind to?

A

Intracellular receptors

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6
Q

Do steroid hormones and T3 act within the nucleus?

A

YES

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7
Q

What happens to the receptor-hormone complex after the hormone binds in the nucleus?

A

Binds to specific DNA sequences to affect transcription

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8
Q

Why can steroid hormones pass through the membrane easily?

A

They are lipophilic because they are derived from cholesterol

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9
Q

Give some examples of the roles of steroid hormones

A

Carbohydrate regulation
mineral balance
reproductive function

inflammatory response, stress response, bone metabolism, cardiovascular fitness, cognition, mood & behaviour

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10
Q

What are most steroid hormones bound to?

A

Plasma protein carriers

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11
Q

What does the hormone receptor complex act as?

A

Transcription factor

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12
Q

Where are thyroid hormones synthesised?

A

Thyroid gland (T4) and peripheral tissues (T3)§ through deiodination of T4

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13
Q

How are thyroid hormones synthesised?

A

An iodine is attached to tyrosine residue son a protein called thyroglobulin. Iodotyrosine molecules in thyroglobulin are cross linked and thyroxine (T4) is cut out.

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14
Q

How do thyroid hormones know where to bind?

A

The thyroid hormone recognition element (RE) is in front of various genes of energy metabolism and heart function

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15
Q

What can thyroid hormone receptor mutation lead to?

A

Thyroid hormone resistance, and symptoms of hypothyroidism

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16
Q

Can you live without either thyroid hormone nuclear receptors?

A

YEs

17
Q

What are nuclear receptors?

A

Sequences upstream of the minimal promoter region in transcription that affect transcription. Some are binding sites for nuclear hormone receptors.
Can include small sequences of 6-10 nucleotides, sometimes with a spacer of a few nucleotides between them. Can be direct repeats (TTAAGGCCXXXTTAAGGCC) or palindrome repeats (TTAAGGCCXXXGTCCTTAA)

18
Q

Is the most efficient response element palindrome or direct repeat? Where is it found?

A

Palindrome

Upstream of an egg protein in Xenopus (frog)

19
Q

What does a steroid hormone receptor consist of?

A 
Variable domain (interacts with other transcription factors)
DNA binding domain (Zinc finger)
Domain for dimerisation (two receptor hormone complexes)
Hormone binding domain
20
Q

How are nuclear receptors activated?

A

Ligand binding which causes conformational change. An inhibitory protein dissociates from the structure and co-activators bind to the complex , forming the hormone receptor complex

21
Q

What is the zinc finger on the nuclear hormone receptor?

A

A zinc atom surrounded by 4 cysteine residues in the groove of the DNA helix stabilises the structure

22
Q

What do thyroid hormones bind to in the nucleus? What do these in turn bind to?

A

thyroid hormone receptors

thyroid response elements

23
Q

What is a homodimer? heterodimer?

A

Thyroid hormone receptors can pair with each other or pair with other nuclear receptors

24
Q

What are the two oestrogen receptors?

Can we live without these?

A

o ERα
o ERβ

Yes

25
Q

What is the difference between thyroid and steroid hormones in terms of DNA binding?

A

Steroid nucelar recpetors wont bind to DNA in the non-activated state

26
Q

How do some retroviruses carry oncogenes? (can cause cancer in organisms they infect)

A

They are often mutated versions of the host cell genes
The retrovirus captures part of a host gene which happens to be a porto-oncogene (important roles in growth but doesnt cause cancer). The partial gene has some biological activity but isn’t subject to normal control.

27
Q

How do oncogenes cause cancer?

A

Proto-onco genes produce proteins that function to stimulate cell division, inhibit differentiation, halt cell death. Oncogenes cause increased production of these proteins = cancer

28
Q

What is androgen sensitivity syndrome? What does it show?

A

Results in the cell’s partial or complete inability to respond to androgens
People are genetically male but have female physical traits

Shows that androgen nuclear signalling is not essential for life

29
Q

How can the hormone progesterone be used in medical therapy?

A

For contraceptives and abortion

30
Q

How can the hormone androgen be used in medical therapy?

A

Prostate cancer

31
Q

How can the hormone oestrogen be used in medical therapy?

A

Breast cancer (tamoxifen)

32
Q

Which oestrogen receptor does breast tissue normally express more of? Which oestrogen receptor does breast cancer express?

A

ERβ

ERα

33
Q

How can breast cancer biopsies be identified

A

Stained with antibodies against the oestrogen receptor (ERα cells are brown)

34
Q

What is the active metabolite of tamoxifen?

A

4-hydroxy tamoxifen

35
Q

What is the normal role of oestrogen?

A

Causes cellular proliferation by binding to oestrogen receptors, causing conformational change and meaning oestrogen receptors can bind to co-activators and bind to DNA

36
Q

How does tamoxifen work?

A

Mimics the shape of oestrogen and binds to oestrogen receptors. No conformational change occurs and the tamoxifen receptor cannot bind to co-actiators so no transcription occurs, tumour shrinks

37
Q

Why is it known that tamoxifen is an agonist in bone and an antagonist in breast?

A

It increases bone density because there is a different receptor (potentially Erβ)

38
Q

What do aromatase inhibitors (MOA) do?

A

They block the formation of the aromatic ring in oestrogen to stop it binding to receptors

39
Q

How can breast cancers become unresponsive to anti-oestrogens?

A

Kinases (e.g. ERK) phosphorylate oestrogen receptor Erα which can activate gene transcription in the absence of oestrogen. This is not blocked by anti-oestrogens.

Developing breast cancers also appear to up-regulate ERK pathways to restore oestrogen-like signalling even in the presence of anti-oestrogens

IMS topic 6 - Endocrinology (4 decks)

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