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Biochemistry > Cellular biology > Flashcards

Cellular biology Flashcards

1
Q

What are the phases of cell cycle?

A

G1——>Go
S
G2
M

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2
Q

What is M phase and its parts?

A

It is the shortest, most rapid phase of cell cycle

Prophase 
Pro metaphase 
Metaphase
Anaphase
Telophase

Cytokinesis

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3
Q

Which phases are of variable duration?

A

G1 and Go

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4
Q

What regulates the cell cycle?

A

Cyclins, CDK, and tumor suppressors

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5
Q

What are the checkpoints?

A

G1—->S

G2—->M

M (prior to anaphase)

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6
Q

How is G1—->S regulated?

A

Mitogens (extracellular proteins, stimulate cell division)

Interact with cell surface receptors

Increase phase sp cyclins

Increase cdk activity (constitutive and inactive, in G1 phase)

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7
Q

What does cyclin cdk complexes do?

A

Phosphorylation of proteins to coordinate cell cycle progression, must be inactivated and activated at app times for cell cycle to progress

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8
Q

What is the function of P53 gene?

A

DNA damage,

P53 (unstable protein, rapid breakdown)

P53 (becomes stabilised)

P53 stimulates p21 gene

P21 protein is formed

Inhibits cdk-cyclin complex

Hypophosphorylation (activation) of rb gene, e2f not activated, G1—->S

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9
Q

What is retinoblastoma?

A

Rare child eye malignancy

Mutations in the Rb1 gene, which codes for abnormal Rb protein—-> unregulated cell growth via e2f

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10
Q

What is the clinical correlation of p53 mutation?

A

Li Fraumeni syndrome (SBLA) (sarcoma, breast, leukaemia, adrenal gland)

Mutation in tp53, abnormal p53, cell cycle not arrested to allow for dna repair, accumulation, malignancy

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11
Q

Permenant cell types are the types that remain in ___________, are terminally differentiated, and regenerate from _________

A

Go

Regenerated from stem cells

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12
Q

What are the examples of permanent cell types?

A

Nerve tissue
Cardiac
Skeletal muscle
RBC

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13
Q

What are stable cell types?

A

Enter G1 to Go when stimulated

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14
Q

What are examples of stable cell types?

A

Liver cells, lymphocytes, pct, periosteal cells

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15
Q

What are labile cell types?

A

Never go to G0, rapidly divide with short G1

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16
Q

Which cell type was commonly affected by chemotherapy?

A

Labile

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17
Q

What are examples of labile cell types?

A

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

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18
Q

Which examples of cells enter and exit G0 many times in their lifetime?

A

Fibroblasts and lymphocytes

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19
Q

Which growth factors have an effect on cell cycle?

A

Insulin, pdgf,epo,egf bind to tyrosine receptors to transition from the G1-S

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20
Q

What is the function of RER?

A

Site of synthesis of exported secretory proteins and N linked oligosaccharide

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21
Q

What are Nissl bodies?

A

They are the rer in neurones. They synthesise peptide neurotransmitters for secretion

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22
Q

What is the function of free ribosomes?

A

Site of synthesis of proteins involved in metabolism and structure

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23
Q

RER are abundant in which structures?

A

Plasma cells, goblet cells, and pancreatic B cells

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24
Q

What are SER?

A

Site of synthesis of steroid, and detoxification of drugs and poisons

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25
Q

SER are abundant in which organelles?

A

Liver hepatocytes
Adrenal cortex
Gonads

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26
Q

What are the modifications that occur in Golgi apparatus?

A

Adding of oligosaccharides to extra N on asparagine

Adding of oligosaccharides to extra O on serine and threonine (mucins)

Adding of mannose 6 phosphate to proteins

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27
Q

What are the endosomes?

A

Sorting centres for material from membrane or Golgi apparatus, fuses with lysosomes, they go back to Golgi apparatus and membranes

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28
Q

What other name is for I cell disease?

A

Mucolipidosis type 11

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29
Q

I cell disease is of which type of genetic disorder?

A

Autosomal recessive

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30
Q

Which enzyme is deficient in I cell disease?

A

N acetylglucosaminyl-1-phosphotransferase

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31
Q

What happens if the enzyme is deficient in I cell disease?

A

Failure of Golgi to phosphorylate mannose residues, so mannose 6 phosphate decreases
Proteins are secreted extra cellularly instead of being transported to lysosomes

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32
Q

What are the symptoms of I cell disease?

A

Coarse facial features, gingival hyperplasia, clouded corneas, restricted joint movements, claw hand deformities, kyphoscoliosis

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33
Q

What are the plasma levels of the lysosomal enzymes in I cell disease?

A

High

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34
Q

What is the future for children in I cell disease?

A

Often fatal in children

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35
Q

What are the functions of peroxisome? Oxidation, catabolism and synthesis wise

A

Beta oxidation of very long fatty acid chains (small in mito)
Alpha oxidation
Catabolism of branched chain fatty acids, aa and ethanol
Synthesis of cholesterol, bile acids and plasmalogens (phospholipid esp in white matter of brain)

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36
Q

Which type of oxidation strictly occurs in peroxisomes regarding fatty chains?

A

Alpha

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37
Q

What is the zell Weger syndrome? Genetic type, mutated gene, symptoms

A

It is an autosomal recessive disorder of peroxisome

Muted pex gene

Hypotonia, hepatotoxicity, seizures, early death

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38
Q

What is refsum disease? Genetic type, defective mechanism, symptoms

A

Defective alpha oxidation, so phytanic acid is not converted into pristanic

Autosomal recessive

Night blindness 
Scaly skin
Ataxia 
Shortening of 4th toe
Epiphyseal dysplasia
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39
Q

What is the treatment of refsum disease?

A

Diet, plasmapheresis

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40
Q

What is adrenoluekodystrophy? Genetic type, defective mechanism,

A

Defect in b oxidation—build up of vlcfa

X linked disorder

White matter of brain, adrenal gland, testes
Leads to adrenal crisis, coma and death

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41
Q

How do proteins from the ribosome go to RER?

______________ are ____________that recognise ____________ from ribosomes and traffic them into RER

A

Signal recognition particle (SRP) are ribonucleoproteins that recognise signal sequences on proteins from ribosomes and traffic them into RER

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42
Q

What would happen in SRPs were deficient?

A

Absent or dysfunctional SRP leads to protein accumulation in cytosol

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43
Q

What are the vesicular trafficking proteins?

A

COP 1, COP 11 and clathrin

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44
Q

What are COP 1?

A

Present on Golgi apparatus

Go from cis Golgi to ER retrograde

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45
Q

What are COP 11?

A

Present on RER

Go from ER to cis Golgi

Anterograde

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46
Q

What are clathrin?

A

Go from trans Golgi to lysosomes

From plasma membranes makes endosomes

LDL receptor on coated pits, plasma membrane invaginates, makes vesicle (receptor mediated endocytosis)

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47
Q

What is a proteasome and what is its use and clinical correlation?

A

Barrel shaped protein complex that degrades ubiquitin tagged proteins. Defects implicated in some cases of Parkinson disease

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48
Q

What are the types of filaments?

A

Microfilaments, intermediate filaments, microtubules

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49
Q

What is the predominant function of microfilament?

A

Muscle contraction, cytokinesis

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50
Q

What are the examples of microfilaments?

A

Actin, microvilli

51
Q

What are intermediate filaments’ predominant function?

A

Maintaining cell structure

52
Q

What is the use of intermediate filaments in laboratory?

A

Immunohistochemistry

Antibodies against intermediate filaments. Positive staining suggest tumour type/origin

53
Q

What are the examples of intermediate filaments?

A

Vimentin, desmin, cytokeratin, lamins, GFAP (glial fibrillary acidic protein), nuerofilaments

VDCLGN

54
Q

Where is vimentin and desmin found?

A

Z disks of sarcomere

55
Q

Which tumors are vimentin implicated in?

A

Sarcoma(mesenchymal origin)(soft tissue)

Leiomyosarcoma, liposarcoma

Non sarcoma tissues

Renal cell carcinoma 
CNS tumors (menangioma)
Endometrial carcinoma
56
Q

Which cancer is desmin implicated in?

A

Positive for muscle tumors

Rhabdomyosarcoma
Leiomyoma
Leimyosarcoma

57
Q

Which cancer is cytokeratin implicated in?

A

Squamous cell carcinoma

58
Q

What is the purpose of lamins?

A

Form nuclear envelope

59
Q

Which cancers is GFAP implicated in?

A

Astrocytoma, glioblastoma

60
Q

Which cancers is neurofilaments implicated in?

A

Nueroblastoma, medulloblastoma, retinoblastoma

61
Q

What is predominant funtion of microtubules?

A

Movement, cell division

62
Q

What are the examples of microtubules?

A

Centrioles, cilia, flagella, mitotic spindle, axonal trafficking

63
Q

What is the basic structure of microtubule?

A

Heterodimer (alpha tubulin, beta tubulin)

Polymerizes into protofilaments

Each dimer has 2 GTP attached

64
Q

What is dynamic instability of microtubules?

A

Grow very slowly

Collapses very quickly

65
Q

What are the microtubule motor proteins?

A

Dynein and kinesin

66
Q

What is dynein?

A

Transports cellular cargo in retrograde fashion (positive to negative) Negative End is Near Nucleus

Involved in axonal flow

67
Q

What is kinesin?

A

Transports cellular cargo in anterograde fashion (negative to positive) postive end points to periphery

Movement of vesicles
Localization of golgi apparatus towards cell centre

68
Q

What is the structure of cilia?

A

Arranged into axonemes:

9 periphery doublet with 2 central doublet

Basal body: it is the base and it is below cell membrane

9 periphery triplet with no central doublet

69
Q

What makes the cilia bend?

A

Axonemal dynein bridges microtubules together, they use atp to pull on neighbouring microtubules——sliding

70
Q

What is the clinical correlation of cilia?

A

Kartagener syndrome (1 ciliary dyskinesia)

71
Q

What is the genetic type disorder of kartagener syndrome?

A

Autosomal recessive

Dynein arm defect

72
Q

What are the symptoms of kartagener syndrome?

A

Recurrent sinusitis

Otitis media (conductive hearing loss)

Female and Male infertility due to immotile sperm and dysfuntional tube

Bronchiectasis

Situs inversus

73
Q

What is the complication of kartagener syndrome?

A

Ectopic pregancy

74
Q

Which is the most abundant protein in the human body?

A

Collagen

75
Q

What are the types of collagen?

A

Type 1, type 11, type 111, type 1V

76
Q

Which type of collagen is the most adundant?

A

Type 1

77
Q

Where is type 1 collagen found in the body?

A

Be So Totally Cool, Chill, Read Books

Bone, Skin, Tendon, Cornea- dentin, fascia

Late wound repair

78
Q

Where is type 11 collagen found in the body?

A

Be So Totally Cool, Chill, Read Books

Cartilage, virtreous body, nucleus pulposus

79
Q

Where is type 111 collagen found in the body?

A

Be So Totally Cool, Chill, Read Books

Reticulin, Blood vessels—-uterus, fetal tissue

Granulation tissue

80
Q

Where is type 1V collagen found in the body?

A

Be So Totally Cool, Chill, Read Books Love

Basement membrane, lens

81
Q

Which collagen type is deficient in Alport syndrome?

A

Type 1V

82
Q

What does the alport syndrome present as?

A

Triad: haemturia, hearing loss, ocular disturbances

83
Q

Which collagen type is targeted by autoantibodies in good pasture syndrome

A

Type 1V

84
Q

What are the steps of collagen synthesis?

A

Synthesis, hydroxylation, glycosylation, exocytosis, proteolytic cleavage, cross linking

Guests, water and lemon, sweets, guests leave

85
Q

What happens in the synthesis step in collagen synthesis?

A

Translation into preprocollagen which is made of alpha chains. Alpha chains Gly-X-Y. Most consists of glycine

86
Q

What happens in the hydroxylation step in collagen synthesis?

A

Hydroxylation of proline and lysine, vitamin c requirement

87
Q

Def of vitamin c will lead to?

A

Scurvy

88
Q

What happens in the glycosylation step in collagen synthesis?

A

Glycosylation of the preprocollagen. Makes good bonds with guests i.e hydrogen and sulphide bonds between preprocollagen into procollagen (triple helix)

89
Q

In which step is the osteogensis imperfecta implicated in collegen synthesis?

A

Glycosylation

90
Q

What happens in the exocytosis step in collagen synthesis?

A

Exocytosis of the procollegen into extra cellular space

91
Q

What happens in the proteolytic cleavage step in collagen synthesis?

A

Cleavage of the C and N terminal ends of the procollagen—-insoluble tropocollagen

92
Q

In which step is the Ehlers Danlos implicated in collegen synthesis?

A

Proteolytic cleavage, and cross linking

93
Q

What happens in the cross linking step in collagen synthesis?

A

Cross linking (lysine hydroxylysine by lysyl oxidase, copper requirement) between tropocollagen—-collagen fibril

94
Q

In which step is the Menkes disease implicated in collegen synthesis?

A

Cross linking

95
Q

What type of genetic disorder is osteogenesis imperfecta?

A

Autosomal dominant is most common form

96
Q

What mutation occurs in osteogenesis imperfecta?

A

COL1A1 and COL1A2

97
Q

Which type of osteogensis imperfecta is more common?

A

Type 1, with decreased production of type 1 collagen

98
Q

What is the severity of the types of OP?

A

Type 2 (lethal in uterus), type 3 and 4, type 1

99
Q

What are the symptoms of OP?

A

Patients cant BITE

bone fractures with minimal trauma—-may occur during birth
Eye- blue sclera, due to translucent sclera over choroidal veins
Teeth- dental imperfections, opalescent teeth that wear easily due to lack of dentin in some forms (dentinogenesis imperfecta)
Ear- hearing loss abnormal ossicles

100
Q

What is Op confused with?

A

Child abuse

101
Q

What can be used to reduce risk of fractures in OP?

A

Bisphosphonates

102
Q

What are the different types of Ehlers Danlos syndrome

A

Classical type, vascular type

103
Q

What mutation occurs in the classical type of Ehlers Danlos?

A

COL5A1 and COL5A2, type 5 mutation

104
Q

What are the symptoms in classical type of ehlers danlos

A

Hypermobile joints, hyperextensibility of skin, easy bruising, mitral valve collapse, thin wide scars

The symptoms may vary in degrees across the types, as they are seen in other types

105
Q

What is deficient in the vascular type of Ehlers Danlos?

A

Type 111 procollagen

106
Q

What are the symptoms in vascular type of ehlers danlos

A

Berry and aortic aneurysm, rupture of large arteries, uterus and intestinal ( hollow) viscera prone to rupture

107
Q

Which form of Ehlers danlos most life threatening?

A

Vascular type

Median age 48

108
Q

What is the inheritance pattern of ED?

A

May be autosomal dom or recessive

109
Q

What inheritance pattern is Menkes disease?

A

X linked recessive

110
Q

What is the mutation in the Menkes disease?
The mutation is in the ______, which leads to decreased _______ protein. This is needed for ________ absorption, needed for ______ activity. There is defective ________

A

ATP7A gene—->ATP7A protein decreased

Needed for copper absorption, low copper, then decreased lysl oxidase activity, defective collagen

111
Q

What are the symptoms in Menkes disease?

A

Brittle kinky hair, hypotonia, growth retardation

112
Q

Where are the elastin located?

A

Skin, lungs, large arteries, elastic ligaments, vocal cords, ligamenta flava

113
Q

What makes elastin different from collagen?

A

Proline, glycine, lysine—-nonhydroxylated

Not glycosylated

114
Q

Where does crosslinking of elastin occur and what does it do?

A

Extra cellular and gives it its elastic properties

115
Q

Which enzyme breaks down elastin?

A

Elastase

116
Q

Which enzyme inhibits elastase?

A

Alpha anti trypsin

117
Q

What occurs in alpha antitrypsin deficiency?

A

Elastase works, which can cause emphysema

118
Q

What changes occur in aging?

A

Decreased dermal collagen and elastin, decreased collagen fibrils

119
Q

Is crosslinking normal in aging?

A

Yes

120
Q

What inheritance pattern is marfan syndrome?

A

Autosomal dominant

121
Q

What mutation occurs in marfan syndrome?

A

FBN1 gene mutation on chromosome 15—-defective fibrillin

122
Q

What is fibrillin?

A

A glycoprotein that forms a sheath around elastin

123
Q

What are the symptoms of marfan syndrome?

A

Skelelton: tall, increased wingspan
Pectus carinatum, pectus excavatum
Arachnodactyl

Heart: floppy mitral valve
Cystic medial necrosis of aorta
Aortic aneurysms

Eye: subluxation of lenses, upward and temporally

(look UP at a ceiling FAN)

124
Q

What is the similarities btw symptoms of marfan and ehlers danlos syndrome?

A

Hypermobile joints
Floppy mitral valve
Aortic aneurysms

Biochemistry (11 decks)

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