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BIOCHEMISTRY > BIOCHEMISTRY- Cellular > Flashcards

BIOCHEMISTRY- Cellular Flashcards

1
Q

Who controls the checkpoints between each transition phase of cell cycle?

A

Cyclins
Cyclin dependent Kinases
Tumor suppresors

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2
Q

Which phase is the shortest in the cell cycle?

A

Mitosis

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3
Q

What phases does Mitosis includes?

A

Profase, Metaphase, anaphase and telophase

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4
Q

Which phases are of variable duration?

A

G1 and G0

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5
Q

During the Regulation of cell cycle, they constitutive and inactive

A

CDKs

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6
Q

Are consider regulatory proteins that control cell cycle events; phase specific

A

Cyclins

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7
Q

In the regulation of cell cycle, this regulatory proteins activate CDKs

A

Cyclins

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8
Q

True or false… is a requirement that the Cyclin -CDK complexes must be both activated and inactivated for the cell cycle to progress

A

True

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9
Q

Two examples of Tumor suppressors

A

p53 and hypophosphorylated RB

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10
Q

What does p53 and hypophosphorylated RB normally do to the cell cycle phases?

A

inhibit G1 to S progression

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11
Q

What happens if there is a mutation for p53 and hypophosphorylated RB genes?

A

Results in unrestrained cell division

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12
Q

Which syndrome is characterized by a unrestrained cell division caused by a mutation for p53 and hypophosphorylated RB?

A

Li-Fraumeni syndrome

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13
Q

What happens during the G phase of the cell cycle?

A

Gap or Growth

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14
Q

What happens during the S phase of the cell cycle?

A

Synthesis

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15
Q

This kind of cell types remain in G0, regenerate from stem cells

A

Permanent

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16
Q

Examples of permanent cells

A

Neurons, skeletal and cardiac muscle, RBCs

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17
Q

This is the main characteristic for the stable cells

A

They enter G1 from G0 when stimulated

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18
Q

Another name for the stable cells

A

quiescent cells

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19
Q

Which ones are example of stable cells?

A

Hepatocytes, lymphocytes

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20
Q

This cells never go to G0, divide rapidly with short G1

A

Labile cells

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21
Q

Give example of cells that are most affected by chemotherapy

A

Bone marrow, gut epithelium, skin, hair follicles, germ cells

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22
Q

Bone marrow, gut epithelium, skin, hair follicles, germ cells… are examples of cells that never go to G0, divide rapidly with short G1, which kind of cells are they?

A

Labile cells

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23
Q

In the cell, it´s the synthesis site of secretory proteins and of N-linked oligosaccharide adition to many proteins

A

Rough endoplasmic reticulum

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24
Q

It´s the name given to RER in neurons, they sinthesize peptide neurotransmitters for secretion

A

Nissl bodies

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25
Q

Which is the function for the free ribosoms?

A

Site of synthesis of cytosolic and organellar proteins

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26
Q

Which kind of cells are rich in RER

A

Mucus secreting goblet cells of small intestine and antibody-secreting plasma cells

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27
Q

Where is the site of steroid synthesis and detoxification of drugs and poisons in the cell?

A

Smooth endoplasmic reticulum

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28
Q

This kind of cells are rich in SER

A

Liver hepatocytes and steroid hormone-producing cells of the adrenal cortex and gonads

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29
Q

Is consider the distribution center for proteins and lipids from the ER to the vesicles and plasma membrane.

A

Golgi apparatus

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30
Q

Who modifies N-oligosaccharides on asparagine?

A

Golgi apparatus

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31
Q

What does the Golgi apparatus adds on serine and threonine?

A

O-oligosaccharides

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32
Q

In the cell trafficking, what does the Golgi apparatus adds to proteins for trafficking to lysosomes?

A

Manosse–phosphate

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33
Q

What is the function for the endosome?

A

They´re sorting centers for material, sending it to lysosomes for destruction or back to the membrane/Golgi for further use

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34
Q

Where do the endosome are localized?

A

Outside the cell or from the Golgi

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35
Q

What kind of disorder is the I-cell disease (inclusion cell disease)?

A

Inherited lysosomal storage disorder

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36
Q

Which is the defect in th I-cell disease?

A

Defect in phosphotranferase

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37
Q

What happens to the Golgi if there is a defect in the phosphotransferase?

A

Failure of the Golgi to phosphorylate manose resideus on glycoproteins

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38
Q

So… if there is a failure of the Golgi to phosphorylate manose resideus on glycoproteins in the I-cell disease, what happens to the proteins?

A

Proteins are secreted extracellularly rather than delivered to lysosomal enzymes

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39
Q

Knowing all the pathophysiolgy of the I-cell disease, what are clinical findings?

A

Coarse facial features, clouded corneas, restricted joint movement, and high plasma levels of lysosomal enzymes

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40
Q

What is the prognosis for the childhood in the I-cell disease?

A

Fatal

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41
Q

If there is an absent or dysfunctional

Signal recognition particle (SRP), what happens to the proteins in the cytosol?

A

The proteins accumulate in the cytosol

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42
Q

In the vesicular trafficking proteins, what is the COPI?

A

It´s a retrograde movement of proteins

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43
Q

What is consider a retrograde movement of proteins in the cell?

A

Golgi→Golgi;

Golgi→Endoplasmic reticulum

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44
Q

What is the COPII, In the vesicular trafficking proteins?

A

An anterograde movement of proteins

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45
Q

What is consider an anterograde movement of proteins in the cell?

A

Golgi→Golgi;

Endoplasmic reticulum→Golgi

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46
Q

Trans Golgi→Lysosomes;
plasma membrane→endosomes
This are a kind of vesicular trafficking proteins

A

Clathrin

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47
Q

Is the LDL receptor activity an example of receptor mediated endocytosis?

A

True

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48
Q

What is the composition of the peroxisome?

A

membrane-enclosed organelle

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49
Q

They´re involved in the catabolism of very-long-chain fatty acids and amino acids

A

Peroxisome

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50
Q

It´s a barrel-shapped protein complex that degrades damaged or ubiquitin-tagged proteins

A

Peroxisome

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51
Q

Which disease is implicated in ubiquitin-protesome system defects?

A

Some cases of Parkinson disease

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52
Q

Which is the structure of the microtubule?

A

Cyclindrical structure composed of a helical array of polymerized heterodimers

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53
Q

In the microtubules, which are the heterodimers that we can find?

A

Alfa and Beta Tubulin

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54
Q

Which kind of bound does each dimer has?

A

2 GTP bound

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55
Q

Where do the microtubules are incorporated?

A

into Flagella, cilia, mitotic spindles

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56
Q

How do you consider the structur of the microtubules?

A

Grow slowly, Collapses quickly

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57
Q

How do the microtubules and the neurons are related?

A

they are involved in slow axoplasmic transport

58
Q

Which Drugs act on the microtubules?

A 
Microtubules Get Constructed Very Poorly
Mebendazole 
Griseofulvin
Colchicine
Vincristine/Vinblastine
Paclitaxel
59
Q

Which kind of filament do the Microtubules have?

A

Protofilaments

60
Q

This are the two types of molecular motor proteins for the microtubules

A

Dynein and Kinesin

61
Q

Which kind of movement does the the Dynein has in the microtubules?

A

retrograde

62
Q

Which direction is the retrograde movement of the dynein?

A

+ → -

63
Q

Manages the anterograde movement in the microtubules

A

Kinesin

64
Q

It has this direction in the microtubule - → +

A

Kinesin

65
Q

Which kind of arrangement does the cilia structure has?

A

9+2 arrangement of microtubules

66
Q

In the cilia this structure links peripheral microtubules and causes bending of cilium by diferential sliding doublets

A

Axonemal dynein-ATPase

67
Q

How many microtubules does the cilia has peripheral?

A

9 doublets

68
Q

How many microtubules does the cilia has centrally?

A

Two

69
Q

Which syndrome is characterized by ciliary dyskinesia?

A

Kartagener syndrome

70
Q

Who in the cilia structure is responsable for the Kartagener Syndrome?

A

immotile cilia due to a dynein arm defect

71
Q

Which manifestations do we see in the reproductive aspect in the Kartagener syndrome?

A

Male and female infertility due to immotile sperm and dysfunctional fallopian tube cilia

72
Q

What risk do the pregnant women has in the ciliary dyskinesia?

A

Ectopic Pregnancy

73
Q

This are other manifestations of the Kartagener syndrome or ciliary dyskinesia

A

Bronchiectases, recurrent sinusitis and situs inversus

74
Q

What is the importance of Actin and myosin?

A

Muscle contraction, microvilli, cytokineses, adherens junctions

75
Q

Long and structural polymers…Who is it actin or myosin?

A

Actin

76
Q

Which form does the myosins have?

A

dimeric

77
Q

ATP-driven motor proteins that move along actins

A

Myosins

78
Q

They´re responsable of the movement, found in the cilia, flagella, mitotic spindle, axonal trafficking and centrioles

A

Microtubule

79
Q

They provide structure. Found in Vimentin, desmin, cytokeratin lamins, glial fibrillary acid proteins (GFAP) and neurofilaments

A

Intermediate filaments

80
Q

Which is the composition of the plasma membrane?

A

Asymetric lipid bilayer

81
Q

In the structurally composition of the plasma membrane, what does it contains?

A

Cholesterol, phospholipids, sphingolipids, glycolipids and proteins

82
Q

What does the Fungal membranes contain?

A

Ergosterol

83
Q

In the immunohistochemical stains for intermediate filaments, where do we find Vimentin?

A

Connective tissue

84
Q

In the immunohistochemical stains for intermediate filaments, we find this in the muscle?

A

Desmin

85
Q

In the immunohistochemical stains for intermediate filaments, we find this in the Neuroglia?

A

GFAP

86
Q

Where is located the ATP site in the NA+-K+ ATPase in the plasma membrane?

A

cytosolic side

87
Q

What happens next, after each ATP is consumed in the sodium-potassium pump, ?

A

3 Na+ go out and 2 k+ come in

88
Q

Which is the effect of the Ouabain if it binds to the Sodio potassium pump?

A

Inhibits by binding to K+ site

89
Q

This are Cardiac glycosides that directly inhibit the Na+-K+ ATPase

A

Digoxin and digitoxin

90
Q

After the direct inhibition of the Na+-K+ ATPase by the Cardiac glycosides, who is indirect inhibited?

A

Na+/ Ca2+

91
Q

If the Na+/ Ca2+ is indirectly inhibited by digoxin and digitoxin, what happens to the calcium and the cardiac contractility?

A

Increase in calcium levels with increase contractility

92
Q

Who is the most abundant protein in the human body?

A

Collagen

93
Q

Which is the most common collagen type?

A

Type I

94
Q

Where do we find Type I Collagen?

A

Found in the bone, skin, tendon, dentin fascia, cornea, late wound repair

95
Q

We find this type of Collagen in Reticulin (skin, blood vessels, uterus, fetal tissue, granulation tissue)

A

Type III

96
Q

Found in the basement membrane, basal lamina, lens

A

Type IV

97
Q

Where do we se Type II collagen?

A

Cartilage (including hyaline), vitreous body, nucleus pulpose

98
Q

This collagen is deficient in the uncommon vascular type of EHler-Danlos syndrome

A

Type III

99
Q

This collagen is decreased in production in osteogenesis imperfecta type 1

A

Type I

100
Q

Which collagen is defective in Alport syndrome?

A

Type IV

101
Q

Which collagen is targeted by autoantibodies in Goodpasture syndrome?

A

Type IV

102
Q

Inside the Fibroblast, where is the site where the collagen is synthesis and structure?

A

RER

103
Q

Name the four phases that occurs inside the fibroblasts to synthesis collagen

A

Synthesis
Hydroxylation
Glycosylation
Exocytosis

104
Q

During the collagen synthesis what is the preprocollagen?

A

Translation of collagen alpha chains

105
Q

Which are the three main components in the collagen synthesis?

A

Gly-X-Y
Glycine
Proline
Lysine

106
Q

From the three main components in the collagen synthesis, which one best reflects collagen synthesis, and becomes 1/3 of collagen?

A

Glycine

107
Q

In the collagen shynthesis who´re the ones that suffer hydroxylation?

A

Proline an lysine residues

108
Q

Which vitamin its required for the hydroxylation during the collagen shynthesis?

A

Vitamin C

109
Q

Name of the disease when there is a Vitamin C deficiency

A

Scurvy

110
Q

Who suffers the glycosylation during the collagen shynthesis?

A

Pro Alpha chain hydroxylisine residues

111
Q

Who forms the triple helix of 3 collagen alpha chains after the Pro Alpha chain hydroxylisine suffers glycosylation?

A

Procollagen via hydrogen and disulfide bonds

112
Q

During the collagen shynthesis, this happens when there is a problem forming tripla helix

A

Osteogenesis imperfecta

113
Q

Who suffers exocytosis to the extracellular space after all the inside fibroblast collagen synthesis?

A

Procollagen

114
Q

What are the two process that happen outside the fibroblast in order to make collagen

A

Proteolytic processing

Cross-linking

115
Q

During the proteolytic process, What happens to procollagen in order to become tropocollagen

A

Cleavage of disulfide-rich terminal regions of procollagen

116
Q

During the Cross linking phase in the collagen synthesis, what kind of bonds need to happen to form the collagen fibrils?

A

Reinforcement of many staggered tropocollagen molecules

117
Q

What kind of bonds does the tropocollagen molecules have with each other to make the collagen fibrils?

A

Covalent lysine-hydroxylysine cross linkage (by Cu2+- containing lysyl oxidase)

118
Q

Which disease has problems with the Cross-linking in the collagen synthesis

A

Ehlers Danlos

119
Q

Which is the most common form of osteogenesis imperfecta?

A

Autosomal dominant

120
Q

Osteogenesis imperfecta manifestations can include

A

Multiple fractures with minimal trauma during the birth process
Blue sclerae
Hearing loss (abnormal ossicles)
Dental imperfections due to lack of dentin

121
Q

Why can we see the blue sclera in the osteogenesis imperfecta?

A

Due to the translucency of the connective tissue over the choroidal veins

122
Q

What´s wrong in Ehlers-Danlos syndrome?

A

Faulty collagen synthesis

123
Q

Which are the most common findings in Ehlers-Danlos?

A

Hyperextensible skin, tendency to bleed and hypermobile joints

124
Q

How many types of Ehlers Danlos can we see?

A

6+ types

125
Q

Which other problems can be associated with Ehlers Danlos?

A

Joint dislocation, berry and aortic aneurysms, organ rupture

126
Q

From all the Ehlers Danlos types, which is the most common?

A

Hypermobility type (joint instability)

127
Q

In Ehlers Danlos, Which collagen is mutated in the Classical type?

A

Type V collagen

128
Q

In Classical type of Ehlers Danlos, which are the common symptoms?

A

Joint and skin symptoms

129
Q

There is a Vascular type of Ehlers Danlos syndrome associated to vascular and organ rupture, which collagen is affected?

A

Type III collagen

130
Q

It consider a connective tissue disease caused by impired copper absortion and transport

A

Menkes disease

131
Q

What happens if the copper is affected in Menkes disease?

A

Leads to decrease activiy of lysyl oxidase (cooper is a necesary cofactor)

132
Q

In Menkes disease, Whiche are the common findings?

A

Brittle, kinky hair
growth retardation
hypotonia

133
Q

Stretchy protein within skin, lungs, large arteries, elastic ligaments, vocal cords, ligamenta flava

A

Elastin

134
Q

Which are the main components for Elastin?

A

Rich in proline and glycine, non hydroxylated forms

135
Q

Which phase gives Elastin its elastic properties

A

Cross-linking that takes place extacellulary

136
Q

Who breaks down the elastin?

A

The elastase

137
Q

Who normaly inhibites the elastase?

A

a1 antitrypsin

138
Q

This syndrome is caused by a defect in fibrillin

A

Marfan syndrome

139
Q

Which glycoprotein forms a sheath around elastin and is affected in Marfan syndrome?

A

Fibrillin

140
Q

We know that emphysema can be cause by a antitrypsin deficiency… so who has excess activity in this disease?

A

Excess Elastase activity

BIOCHEMISTRY (12 decks)

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