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AU13 Biochemistry Final > Smith - Cellular Homeostasis > Flashcards

Smith - Cellular Homeostasis Flashcards

1
Q

In unicellular organisms:
primary limitation on proliferation is availability of _______ and _______
natural selection favors the cells that ______ more
more division = more mutations = faster ______
when a cell can no longer divide the organism _____

A

nutrients and energy
divide
evolution
dies

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2
Q

In multicellular organisms:
vast majority of cells are ____ dividing, regardless of availability of nutrients (stop dividing when they bump against one another
______ controls on different cell types
more divisons = more mutations = more _______
when a cell can no longer divide the organism must ___ ______
____ ____ is controlled

A 
not
different
problems
be replaces
cell death
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3
Q

In the cell cycle, the cell first ______ its contents, then ______ into ____ _____ ______

A

duplicate
divides
two daughter cells

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4
Q

The division part of the cell cycle is called ______, and usually lasts about _____

A

mitosis

one hour

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5
Q

_____ phase is where there is the most variability among cell types

A

G1

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6
Q

The length of _______ determines the length of the cell cycle, with ____ being the greatest determinant

A

interphase

G0

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7
Q

The checkpoint at ____ is to ensure if the environment is favorable for division

A

G1

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8
Q

The checkpoint at ___ is to check is the environment is favorable AND that DNA is duplicated; and the cell with undergo apoptosis if not

A

G2

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9
Q

The checkpoint at ______ is to ensure the chromosomes are attached to the spindle

A

metaphase

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10
Q

_______ are normal cellular genes that function in cell proliferation

A

protooncogenes

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11
Q

Protooncogenes have a _____ mutant phenotype; cellular transformation occurs with a mutation in ____ allele

A

dominant

one

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12
Q

A mutated protooncogene is called a ______

A

oncogene

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13
Q

______ _____ _____ are anti proliferative genes

A

tumor supressor genes

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14
Q

Tumor supressor genes have a _____ mutant phenotype; loss of expression in _____ allele leads to uncontrolled cell division

A

recessive

both

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15
Q

_____ _____ are signals for proliferation, usually several work in concert to stimulate cell division; do not induce division, bind to specific cell receptors thus involved in signal transduction pathways, PDGF is the model

A

growth factors

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16
Q

How cells respond to PDGF (platelet derived growth factor):
increase in intracellular ____ ions
reorganization of ___ stress fibers to facilitate attachment
activation and nuclear translocation of _____ _____
____ synthesis and _____ division

A 
calcium
actin
transcription factors
DNA
cell
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17
Q

Growth factors: PDGF

growth factor + growth factor receptor –> receptor _________

A

oligomerization

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18
Q

Growth factors: PDGF

receptor oligomerization —> receptor ____ activation (intrinsic = ______; extrinsic = ______)

A

PTK (protein tyrosine kinase)
part of receptor
separate protein that associates with receptor

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19
Q

Growth factors: PDGF

receptor PTK activation –> ______ of PTK moiety —> docking sites form

A

phosphorylation

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20
Q

Growth factors: PDGF

once docking sites form —> _______ of signaling enzymes —> activation of _____ _____

A 
recruitment
signal transduction (ST) elements
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21
Q

PTKs transfer a __________ group of ATP to _________ residues on target substrate proteins

A

γ-phosphate

tyrosine

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22
Q

Tyrosine phosphorylation, which is a covalent modification of proteins, provides a _________ and ________ (by the action of protein tyrosine phosphatases) mechanism of modifying the enzymic activity of target proteins.

A

rapid

reversible

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23
Q

The importance of PTKs in cell _______ and ________ function is illustrated by the defects resulting from _________ in these genes occurring in humans

A

proliferation
effector
mutations

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24
Q

Mutations in ______ can result in severe combined immunodeficiency (SCID) due to severe abnormalities in T cell development, X-linked agammaglobulinemia, an immunodeficiency characterized by lack of IgG antibody production, chronic myeloid leukemia (CML), acute lymphoblastic leukemia (ALL), and occasionally in acute myeloid leukemia (AML)

A

PTK

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25
Q

Docking sites created by PTK can lead to recruitment of _______ _______ enzymes, specifically PLC and GAP

A

downstream signaling

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26
Q

PDGF is a ______ ______ receptor, it involves ________ and _____-____ cascades, it is involved in the recruitment of _____, the second messengers are _____ and ______, and its molecular switch is ______

A 
membrane bound
phosphatidylinositol
Ras-MAPK
PLC
IP3 
DAG
Ras
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27
Q

If Ras is on then _____ undergoes uncontrolled division; because Ras regulates the _____ pathway, which is involved in the regulation of DNA synthesis and cell division (TF activation)

A

MAPK

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28
Q

Grb2 and Sos recruit _____ and is inactive due to GDP; _____ promotes the activation of _____ whereas ____ inactivates ____ by stimulating its intrinsic ______ activity

A 
Ras
Sos
Ras
GAP
Ras
GTP
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29
Q

______ of all tumors have mutation in ____ that render it constituently active

A

30%

Ras

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30
Q

With cytokines; hemopoietic receptors are ____ _____, JAKs couple the receptor directly to ________, STATs ________ in cytoplasm then translocate to the nucleus to activate _______

A

membrane bound
transcription
phosphorylated
transcription

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31
Q 
True or False
The following are key regulators of the cell cycle:
cyclin/CDK complexes
retinoblastoma protein (Rb)
p53 (tumor supressor gene)
CDKIs
E2F family of Tfs
A

True

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32
Q

Cyclin/CDK (cyclin dependent kinses)
the _______ of cyclins via mRNA/protein levels
the _______ on CDKs via phosphorylation and CDKIs
A CDK can have _____ activities when interacting with different cyclins

A

abundance
activity
differing

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33
Q

Growth factors usually exert effects between the onset of ____ and the _____ _____ (late G1)

A

G1

restriction point

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34
Q

Once past the restriction point, the rest of the phases up to mitosis are ______, but not ______

A

committed

unregulated

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35
Q

_________ is the gatekeeper of the restriction point

A

retinoblastoma (Rb)

36
Q

In early G1, ______ prevents transcription factors, closer to the restriction point _________ phosphorylates _____; hyperphosphorylated _____ releases TFs allowing the cycle to pass the restriction point

A

Rb
cyclin D-CDK4
Rb
Rb

37
Q

If damage is detected during the cell cycle, ________ induces unphosphorylation of Rb

A

CDKI p21

38
Q

In S phase, ______ monitors for damage

A

p53

39
Q

While committed, the cell cycle can be _____ ____ beyond the restriction point if DNA needs to be repaired

A

slowed down

40
Q

Irreparable damage during cell cycle = ________

A

apoptosis

41
Q

In apoptosis; inappropriate cell death can lead to _________ disorders, subversion of cell death leads to _____ or ______ disease

A

degenerative
cancer
autoimmune

42
Q

In apoptosis, caspases are _________,

______ is a regulator and its antiapoptotic

A

proteases

Bcl-2

43
Q

Cell death domains attract ________ which induce _____ _____ activation cascade, causing apoptosis; survival factors stimulate ______ which inactivate _______ allowing the cell to survive

A

procaspases
proteolytic caspase

Bcl-2
caspases

44
Q

Hyperphosphorylation and inactivation of Rb leading to deregulated malignant cell proliferation leads to ______ cancer(s)

A

breast

45
Q

Loss of Rb control of cell cycle, leading to deregulated malignant cell proliferation leads to _____ cancer(s)

A

retinoblastoma(s)

46
Q

Loss of Rb control of cell cycle leads to ______ cancer(s)

A

cervical

47
Q

Loss of inhibition of cyclin D-CDK4/6 complexes, resulting in inappropriate hyperphosphorylation and inactivation of Rb leads to ______ cancers

A

many; a variety of tumor cells

48
Q

Loss of inhibition of cyclin D-CDK4/6 complexes, resulting in loss of Rb control of cell cycle leads to _______ cancer(s)

A

melanomas

49
Q

Each tumor originated from a _____ mutant cell(s) that outgrew its neighbors

A

single

50
Q

The normal mutation rate = _____/cell divison

A

10 to the 6th

51
Q

Several _____ mutations have to occur over a lifetime, which is why cancer increases exponentially with ____; usually ___-___ mutations required

A

rare
age
3-7

52
Q

90% of human cancers are ________

A

carcinomas

53
Q

Cancer of the epithelial tissue type is _______

A

carcinoma

54
Q

Cancer of the connective tissue or muscle tissue type is ________

A

sarcoma

55
Q

Cancer of the hematopoietic tissue type is ________

A

leukemia

56
Q

_______ were first identified as viral genes that infect normal cells and lead to transformation

A

oncogenes

57
Q

C-Src protooncogene is a ______ involved in normal cell growth (removes introns)

A

PTK

58
Q

Viral oncogene is a _____ _____ of normal cellular gene

A

mutated homolog

59
Q

A gene can come under control of a _______ ______ or _____ that a virus introduces into the genome

A

constitutive promoter

enhancer

60
Q

Insertion of a ______ can cause activation of a protooncogene

A

retrovirus

61
Q

85% of human tumors arise from _____ _____ or ______ in oncogenes

A

point mutations

deletions

62
Q

In _______ cancer, 50% of these tumors had an activating point mutation in a Ras oncogene, and 75% of these cancers had an inactivating mutation in p53; loss of the DNA-damage sensing function of p53 allows the cells to accumulate, at a rapid rate (these mutations appear to be the rate-limiting steps)

A

colorectal

63
Q

_______ are extremely rare; the hereditary form results from a deletion or loss of function mutation of the Rb gene in _____ cell
In the non-hereditary form, both copes are defective in cancer forms

A

retinoblastomas

every

64
Q

The most common genetic lesion found in human cancer is in ____

A

p53

65
Q

Individuals with only one functional _____ are predisposed to sarcoma, lung, breast, larynx, and colon cancers, brain tumors, and leukemias

A

p53

66
Q

True or False
Signs and symptoms of oral cancers can be;
white or red patches in the mouth, a mouth sore that doesn’t heal, bleeding, loose teeth, painful swallowing, a lump in the neck, and an earache

A

True

67
Q

True or False

Oral cancer count for roughly 20% of all malignant lesions worldwide

A

False; only about 5%

68
Q

True or False

The 5-year survival rate of oral cancer is ~80%

A

False; the survival rate is only 50% mostly due to late detection

69
Q

The majority (96%) of oral cancers are ________

A

carcinomas

70
Q

Most oral cancers are _______ cell carcinomas that tend to ______ ______

A

squamous

spread quickly

71
Q

True or False

Oral cancers rank #10 in the global cancer burden

A

False; they rank at #5

72
Q

True or False

Oral cancers may require surgery, radiation, or chemotherapy (or a combination of them all)

A

True

73
Q

True or False

Smoking/tobacco use is associated with nearly 90% of all oral cancer cases

A

False; it is associated with ~75%

74
Q

True or False
Besides smoking/tobacco use, other risk factors for oral cancer include heavy alcohol use, HPV, chronic irritation, immunosuppressants, and poor dental/oral hygiene

A

True; most cancers arise from a combination of different risk factors

75
Q

________ converts nicotine to cotinine which is glucuronidated and then enters the bloodstream

A

CYP2A6 (cytochrome P450s)

76
Q

in the body, ______ can be oxidized and will act as an alkylating agent, leading to DNA damage

A

amines

77
Q

_____ are ROS

A

NOs

78
Q

_____ mutation = oral cancer from smoking

A

GST

79
Q

Extra-hepatic metabolism of alcohol to acetaldehyde is particularly shown to occur in oral cavity, acetaldehyde is __________, and increases ______ permeability; heterozygous genotype substantially predisposed to esophageal cancer

A

mutagenic

mucosal

80
Q

______ interferes with DNA repair enzymes; oral microflora produces a considerable amount (streptococci)

A

acetaldehyde

81
Q

______ decreases secretions from parotid glands

A

alcohol

82
Q

There is mounting evidence that _____ in ______ is causing a predisposition to oral cancer

A

alcohol in mouthwash

83
Q

____ is more often a cause of oral cancer than smoking

A

HPV

84
Q

HPV-16 immortalized cells express higher _____ enzymes; significantly higher concentrations of the _______ compound derived from nicotine in the cervical mucosa of smokers; thus more likely to have carcinogenic nitrosamines produced in those cells

A

P450

butanone

85
Q

HPV E6 interacts with ____ preventing commitment to apoptosis

A

p53

86
Q

HPV E7 binds to ___ preventing damaged cell growth stoppage

A

Rb

87
Q

HPV E5 inhibits ATPS involved in ________ function, delaying endosomal litigation, delaying the response to ____

A

lysosomal

ROS

AU13 Biochemistry Final (14 decks)

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