PRIN 4 Organization of the Cell Flashcards

1
Q

diastrase

A

enzyme that digests glycogen

*was used to clear the liver biopsy sample of glycogen. As a result, PAS allows visualization of the glycosylated granules of alpha1-proteinase inhibitor that was defective and trapped in the rER

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

Plasma vs Serum

A

PLASMA: contains all clotting factors
SERUM: after clotting factors have been removed

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

What is “Alpha-1 antitrypsin?”

A
  • protein that is produced mostly in the liver

* protects the lungs from neutrophil elastase

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

What is “Neutrophil elastase?”

A
  • enzyme that digests damaged or aging cells and bacteria in the lungs
  • regulated by alpha 1 proteinase inhibitor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the result of alpha1-proteinase inhibitor def?

A

Elastase digests lung tissue in an uncontrolled fashion and leads to emphysema
***HIGH risk of lung disease

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

How is Kartageners Syndrome inherited?

A

Autosomal recessive mutation

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

What causes Kartageners Syndrome?

A

loss of dynein arms: cilia don’t work properly

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

Clinical Manifestation of Kartageners Syndrome:

A

(1) recurrent upper resp infections
(2) male infertility
(3) ectopic preg
(4) organs on wrong side

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

What causes CF?

A
Cystic Fibrosus
Autosomal recessive (CFTR gene)
*Defect in ABC transporter (ATP-binding cassette) results in faulty transmembrane protein that is an epithelial Cl- channel
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What happens to the faulty CFTR gene in CF?

A

gets degraded by proteosome

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

Newly made proteins leave the rER and go where?

A

cis face of golgi via vesicle with COP2 coat

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

How do vesicles get BACK to the golgi?

A

via COP1 coat

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

What is the “H-antigen?”

A

*protein that is expressed on RBC membrane surfaces

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

What is glyco-syl-transferase?

A
  • protein that modifies H-antigen on RBC surfaces

* exists in 3 forms depending on the 3 allele forms: ABO

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

What does the O allele result in?

A

encodes for an inactive glyco-syl-transferase leaving the H antigen unmodified

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

Example of Regulated Secretion

A

(1) Synaptic Transmission
(2) Mast Cell
(3) Salivary Glands

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

How is exocytosis regulated in Synaptic Transmission?

A

V-SNARE on vesicle interacts with T-SNARE on target

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

How do tetanus toxins disrupt synaptic transmission?

A

cleave SNARES preventing interaction and release of contents into synaptic cleft

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

How does hay fever result in allergies?

A

Hay fever toxins mimic IgE and bind & stimulate release of Mast Cell granules

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

What causes scurvy?

A

Lack of Vit C

Vit C is involved in recycling of enzyme proline hydroxylane which is needed to make collagen in rER

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

Proteosome vs Lysozome

A

PROTEOSOME: recycling of intracellular cytoplasmic materials

LYSOSOME: digestion of endocytized material

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

Orientation of Hepatocyte

A

BASAL: Sinusoids (Hepatic Artery branch & Portal Vein branch)

APICAL: Secrete bile into Bile Canaliculi which flows into Bile Duct

23
Q

Cytoskeleton Sizes

A

Microfil: 5-9nm
Int. Fil: 10-12nm
Microtub: 25nm

24
Q

Name for Intermediate Filaments in epithelia

A

Keratins

25
Q

Name for Intermediate Filaments in Muscle

A

Desmin

26
Q

Name for Intermediate Filaments in CT

A

Vimentin

27
Q

Name for Intermediate Filaments in neurons

A

Neurofilaments

28
Q

What are the roles of Microtubules?

A

(1) moving cargo around cell
(2) cilia (bronchials, sperm)
(3) spindle formation

29
Q

Cell-Cell Attachments

A

(1) ZONULA ADHERINS (cadherins, catenin, actin)
(2) ZONULA OCCLUDENS (tight junctions)
(3) DESMOSOMES (macula densa)
(4) GAP JUNCTIONS (via connexons)

30
Q

How to recognize Microtubules on EM?

A

They are HOLLOW

31
Q

What does “Zonula Adherens” mean?

A

Zonula = Belt

cadherins, catenin, actin

32
Q

Descibe the Core Junction Complex in cells

A

Receptors: cadherins
Linkers: Catenins
Cytoskeleton: Actin

33
Q

Why are Cadherins so important for development?

A

Each tissue has specific cadherins so that they stick to only those of similar kind

34
Q

What do Catenins do?

A

(1) LINK cadherins to actin cytoskeleton

(2) signal transduction

35
Q

Where are desmosomes located?

A

usually more basal than Zolulas but can be located anywhere along lateral surface

36
Q

How are desmomes linked?

A

linked to stable intermediate filaments

**provide tensile strength

37
Q

Structure of Gap Junctions

A

Connexins = pores

38
Q

Cell-ECM Attachments

A

HEMIDESMOSOMES (stable)

FOCAL ADHESIONS (dynamic)

39
Q

What do Hemidesmosomes anchor to?

A

Basal Lamina

40
Q

What do Focal Adhesions do?

Example?

A
  • migrate according to kinase activity

* Movement of neurons to extend their dendrites to form new synapses

41
Q

What is the role of APC?

A

APC (tumor supp.) roams the cell and sends loose B-catenin to the Proteosome.
(Wnt turns of APC)

42
Q

What gives microvili their shape?

A

Actin

43
Q

Invagination vs Evagination

A

Invagination: infolding of one part within another part of a structure

Evagination: obtrusion of a layer or part to form a pouch.

44
Q

Why can’t a protein that is normally synthesized on the rough ER be translated in the cytosol and THEN enter the ER lumen?

A

Proteins must cross into the ER as they are being synthesized

45
Q

Hyperplasia vs Hypertrophy

A
Hyperplasia = increase in number of cells
Hypertrophy = increase in size of cells
46
Q

Hemidesmosomes VS Focal Adhesions

A

Hemidesmosomes = static

Focal Adh = dynamic

47
Q

What can cause tissue enlargement?

A

(1) Hyperplasia
(2) Hypertrophy
(3) Increase in ECM
(4) Increased Perfusion
(5) Inflammation
(6) Inc spaces between cells
(7) Scarring/fibrosis

48
Q

Why does repeated elastase activity reduce the total amount of lung elastin over time?

A

elastin synthesis essentially ceases after the age of about 18 years

49
Q

Variants of a1 anti-trypsin

A

MM - normal pop
MZ - hetero (Lucy’s parents)
ZZ - Lucy

50
Q

Where does Protein synthesis of lysosomal enzymes occur?

A

rER

51
Q

What is the function of Clathrin-coated vesicles?

A

Transport from trans face of the Golgi apparatus to lysosomes and from the PM into the cell.

52
Q

How and where are Lysosomal enzymes produced?

A

Lysosomal enzymes are synthesized in rough ER and are targeted through the Golgi before ending up in lysosomes.

53
Q

True or False:

Alpha-1-antitrypsin is a neutrophil enzyme that degrades elastin in the lungs

A

FALSE … here’s the truth:

Alpha-1-antitrypsin: proteinase inhibitor

Elastase: neutrophil enzyme