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Membranes and Receptors > Lecture 2.2: Receptor Mediated Endocytosis > Flashcards

Lecture 2.2: Receptor Mediated Endocytosis Flashcards

1
Q

What is Endocytosis?

A

It is the process by which substances enter a cell through the process of engulfment

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2
Q

What are the 3 Types of Endocytosis?

A
  • Phagocytosis (cell eating)
  • Pinocytosis (cell drinking)
  • Receptor mediated endocytosis (RME)
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3
Q

Why is RME important?

A

It allows the internalisation of membrane receptors and their ligands via a membrane invagination process

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4
Q

What types of substances may be transferred in endocytosis?

A
  • Nutrients
  • Growth Factors
  • Viruses
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5
Q

What is Phagocytosis?

A

It is the recognition, binding, internalization and destruction of large particles (cells, bacteria, viruses) >0.5μm

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6
Q

What cells specialise in Phagocytosis (Phagocytes)? (3)

A
  • Macrophages
  • Polymorphonuclear Neutrophils
  • Dendritic Cells
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7
Q

What is the mechanism of phagocytosis?

A
  • Pseudopodia form around the particle
    forming a phagocytic vacuole. Also called a
    phagosome
  • The phagosome fuses with a lysosome (or
    late endosome) and form a
    phagolysosome
  • Particle is hydrolysed
  • Useful parts retained in cell, debris is
    released from cell via exocytosis
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8
Q

How do phagocytes recognise pathogens?

A

They have PRRs which recognise PAMPs associated with microorganisms

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9
Q

What are PRRs?

A

Pattern Recognition Receptors

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10
Q

What are PAMPs?

A

Pathogen Associated Molecular Patterns

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11
Q

What are the 4 families of PRRs?

A
  • Toll-like receptors (TLR)
  • Nucleotide-binding oligomerization
    domain-like receptors (NLR)
  • C-type lectin receptors (CLR)
  • RIG-1 like receptors (RLR)
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12
Q

What does TLR4 recognise?

A

The lipopolysaccharide component of the cell wall of Gram-ve bacteria

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13
Q

What other receptors do Phagocytes have? Why are these important?

A
  • Receptors for the Fc (heavy chain) end of
    IgG molecules and for the C3b fragment of
    complement
  • They use these to recogniSe and ingest IgG-
    or C3b-coated targets
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14
Q

What is Opsonisation?

A

An immune process which uses opsonins (i.e. IgG) to tag foreign pathogens for elimination by phagocytes

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15
Q

What is another name for receptor mediated endocytosis?

A

Clathrin-dependent endocytosis

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16
Q

What is receptor mediated endocytosis?

A

It is the primary process by which cells internalise macromolecules such as hormones, enzymes, plasma proteins, cholesterol, iron…etc

17
Q

What is the mechanism of receptor mediated endocytosis? (8 Steps)

A

1) Ligand binds to membrane receptor
2) Receptor-ligand migrates to clathrin-coated pit
3) Endocytosis
4) Vesicle loses clathrin coat
5) Receptors and ligands separate
6) Ligands go to lysosomes or Golgi for processing
7) Vesicle with receptors moves to the cell membrane
8) Transport vesicle and cell membrane fuse
(membrane recycling)

18
Q

How is cholesterol transported in the blood?

A

In lipoproteins

19
Q

What are Apolipoprotiens?

A

Apolipoproteins are proteins that bind to lipids (fats)

20
Q

What is the role of Apolipoprotiens?

A
  • To bind to and effectively solubilise lipids in
    the blood
  • Combine with phospholipids to form
    lipoprotein particles
  • Different lipids can be packed into these
  • They also have a critical role as ligands
21
Q

What Apolipoprotien is necessary for binding of LDL to LDL receptors and therefore its removal from circulation?

A

ApoB-100

22
Q

What is Familial Hypercholesterolemia?

A

A genetic disease that causes high cholesterol levels in blood due to a defect in the LDL receptor (LDLR)

23
Q

5 major classes of FH due to LDLR mutations: Class I

A

LDLR not synthesised

24
Q

5 major classes of FH due to LDLR mutations: Class II

A

LDLR not transported from ER to Golgi for expression on the cell surface

25
Q

5 major classes of FH due to LDLR mutations: Class III

A

LDLR does not bind LDL on cell surface because of a defect in either apolipoprotein B100 or in LDLR

26
Q

5 major classes of FH due to LDLR mutations: Class IV

A

LDLR bound to LDL does not cluster in clathrin-coated pits for receptor mediated endocytosis

27
Q

5 major classes of FH due to LDLR mutations: Class V

A

LDLR is not recycled back to the cell surface

28
Q

What are the clinical presentations of hypercholesterolemia? (3)

A

Xanthelasma
Corneal Arcus
Xanthoma

29
Q

What is Transferrin?

A

It is a plasma glycoprotein that reversibly binds iron

30
Q

What is the role of Transferrin?

A

It is a major mediator of iron homeostasis

31
Q

What is iron binding to Transferrin dependent on?

A

It is pH dependent, low pH reduces affinity and favours apotransferrin

32
Q

Mode 1 of Receptor-Mediated Endocytosis: Fate of Receptor? Fate of Ligand? Example?

A

Receptor: Recycled
Ligand: Degraded
Example: LDL

33
Q

Mode 2 of Receptor-Mediated Endocytosis: Fate of Receptor? Fate of Ligand? Example?

A

Receptor: Recycled
Ligand: Recycled
Example: Transferrin

34
Q

Mode 3 of Receptor-Mediated Endocytosis: Fate of Receptor? Fate of Ligand? Example?

A

Receptor: Degraded
Ligand: Degraded
Example: Insulin, Epidermal growth factor Immune complexes

35
Q

Mode 4 of Receptor-Mediated Endocytosis: Fate of Receptor? Fate of Ligand? Example?

A

Receptor: Transported
Ligand: Transported
Example: Maternal immunoglobulin G,
Secretory immunoglobulin A

36
Q

What is Transcytosis?

A

It is the transport of molecules across the cytoplasm of a cell, it consists of endocytotic uptake and exocytotic release

37
Q

How is B12 absorbed?

A
  • B12 in mouth binds to haptocorrin
  • HCl in the stomach separates vitamin B12 from the
    protein that it’s attached to
  • The freed vitamin B12 then combines with a protein
    made by the stomach, called intrinsic factor
  • The body absorbs them together in the gut

Membranes and Receptors (19 decks)

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