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2 Weeks > terms 11.1 > Flashcards

terms 11.1 Flashcards

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1
Q

adenylate

A

aa+AMP
formed in the charging reaction of the
fisrt stage

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2
Q

tryptophanyl trna synthetase

A

aminoacyl trna synthetase aa here is trp

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3
Q

aminoacyl AMP,

A

adenylate aminoacid

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4
Q

shine dalrgarno

A

purine /ga rich sequence in mrna of prok

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5
Q

resolution in the holliday model

A

=cleabage
horizontal= non-cross over,patched recombination ,nick already cut
vertical= cross over , spluced recombination
nick unbroken strand

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6
Q

, SPO11

A

ntroduces the double strand breaks
in high number during the meiotic prophase

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7
Q

secondary
structures at DNA repeats

A

(replicative slippage

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8
Q

DARS

A

DUFY ANTIGEN RECEPTOR CHEMOKINES PR

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9
Q

SICKLE CELL AND MALARIABA

A

BALANCE SELECTION

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10
Q

G6PD AND MALARIA

A

RECENTLY + SELECTION

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11
Q

LACK OF DARS/DUFFY ANTIGEN / FY*O AND MALARIA

A

RECENTLY NEGATIVE

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12
Q

IF VS TF

A

IF = INITATION FACTOR =TRANSLATION
TF=TRANSCRIPTION FACTOR =TRRANSCRIPTION

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13
Q

FMET-TRNAIFMET

A

INITITATOR TRNA CARRYING FORMYL METHIONINE FOR STRATING THE TRANSLATION FROM THE P SITE

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14
Q

ELF4

A

CAP BINDING PR

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15
Q

AGGREGATE FACTORS IN INITITATION TRANS;LATION

A

ELF4A AND ELF4B-HELP THE SCANNING - PROVIDE THE HELICASE ACTIVITY

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16
Q

KOZAK SEQUENCE

A

CONSENSUS SEQUENCE FOR IDENTIFIACTION OF THE RIGHT AUG ! IN EUK 5 PRIME R NNAUGG….5 PRIME

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17
Q

recquirment 60s subunit

A

release of elf5b and hydrolyzation additional gtp

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18
Q

elf4

A

bind to capping site of the mrna
consist of elf4e , elf4g and elf4a

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19
Q

pABP

A

POLY A BINDING PR

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20
Q

AMINOACYLATED TRNA

A

AA+TRNA

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21
Q

SOURCES OF INFLAMMAGEING

A

1) endogenous self-derived debris that accumulate
during ageing à dead cells and damaged
organelles,
2) senescent cells and cells which harbour a
DNA damage and are capable of a “DNA damage
response” that secrete a variety of proinflammatory cytokines that alter the
microenvironment
3) persistent infections that accelerate
immunosenescence (CMV, EBV

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22
Q

REMODELLING THEORY OF AGING

A

adaptation of the body to continuous stimuli and stressors occurring over time

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23
Q

perturbations

A

آشفتگی ها

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24
Q

frailty

A

weakness and lack of health or strength:

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25
MRP
(maximum reproduction potential
26
APOE
anp 4 related to atgoistic pleiropy erly life : clear nfection more- eneregtic contraint - energy for gowth of child later disrupts lipid metabolism in neurons and astrocytes (brain cells that support neurons) and significantly reduces microglial activity, whose primary function is the removal of unwanted entities, ranging from pathogens to waste amyloid protein
27
if2 favor binding
fmet-trnaifmet
28
if3 favor binding
mrna
29
peptide bond in transalton happen between ....and ....
new aa and nascentchairn carboxyl group
30
EF-TU
ELONGATION FACTOR IN THE TRANSALTION PROMOTE THE AMINOCYL TRNA ON THE SITE OF RIBOSOME
31
DECODING CENTER
MINOR SUBUNIT 16S EXCLUSIVLEY
32
EF-TS
RECYCLINF THE GDP TO GTP THERORRE ACTIVATION OF THE EF-TU
33
EF-G
GTP DEPENDENT BIND TO A SITE ACTIVATES THE TRANSLOCATION
34
2 MOLECCULES OF MMICRY
EF-G AND EF-TU AND RF3
35
CLASSSIFICATION OF THE RELEASE FACTORS
CLASS1 = RECOGNATION STOP CONODNS RF1 AND RF2 CLAASS 2= STIMULATION OTHER RF-PROMOTE THE RELEASE -RECYCLE -RF3
36
RF1 RECOGNISE
RELEASE FACTOR OFF TRANSLATION IN THE PRO UAA,UAG
37
RF2
RELEASE FACTOR OF THE TRSNALATION UAA , UGA
38
GGQ MOTIF
onserved mechanism of translation termination, CONSERVED IN ALL 3 RELEASE FACTORS
39
👕 SIRTs⇧(sirtuins )
-enzyme -features : in aging :repair damaged DNA, genome stability⬆ modulate cellular responses to stress ⇓ maintenance of cellular and genomic integrity. Age ↑ → efficiency of the SIRTS and its function ⬇ = contribute aging phenotype _ factors influenced on the activity :caloric restriction→ increase the expression and activity of sirtuins→enhanced cellular repair mechanisms→slowing down the aging process.
40
🦊FOXO⇧
-pr - including FOXO1, FOXO3, FOXO4, and FOXO6 -function : DNA repair, apoptosis (programmed cell death), cell cycle control, and oxidative stress response(activation of antioxidant defenses→repair mechanisms→cope with various stressors related to aging ) -increase the foxo ∝increase longevity. -negative regulation = insulin and IGF
41
AMPK
enzym -when activate? deplete cellular energy levels, ex : no nutrient lots of energy expenditure -function : 1- sensor of cellular energy status⇒ cellular energy homeostasis 2- during aging: AMPK activation→ enhance mitochondrial biogenesis(beacuse mit efficiency decreases sue aging) → improved cellular energy metabolism→ extended longevity /decrease the aging 3- autophagy stimulation → removal of damaged or dysfunctional cellular components → extended longevity /decrease the aging *:Autophagy is crucial for maintaining cellular health, and its decline is associated with aging
42
enzymes with hihger longevity
AMPK,FOXO,SIRTS
43
IGF1 INSULINE
Insulin-like Growth Factor 1 Similar structure to insulin Peptide like hormone -function : during childhood and adolescence growth and development, development of bones, muscles, and other tissues Negative control of the FOXO factors -production : response to growth hormone stimulation→prduce in liver -Elevated levels⇾ increased risk of certain age-related diseases, including cancer ⇒reducing the activity ∝extend lifespan
44
Rapamycin
45
ECOLOGICAL DIMENSION
tudy of how the natural environment affects the aging process
45
🛵mTOR
Mechanistic Target of Rapamycin
46
TEMPORAL DIMENSION
study of how the pace of aging changes over time.
47
4E-BP
INHIBITOR OF THE EIF4E IF IT GETS PHOPHOPHORYLATION BY GROWTH FACTOR IT INCREASE THE TRANSLATION
48
BAR PHENOTYPE IN DROSOPHILA
X LINKED DUPLICATION
49
DOUBLE BAR
THREE COPIES OF THE BAR DUPLICATION DOSAGE AND POSITION
50
CGH
Comparative Genomic Hybridization
51
PARACENTRIC
TYPE OF INVERSION DOESNT INVOLVE THE CETROMERE
52
PERICENTRIC
TYPE OF INVERSION INVOLVE THE THE CENTROMER
53
DICENTRIC AND ACENTRIC
HAPPEN DURING THE INVERSION IN PARACENTRIC ONE OF THE CHROMATID HAS NO CENTROMER AND THE OTHER ONE 2 CENTROMERS
54
RSULT OF PARACENTERIC HETEROZYGOTE CROSS OVER
NON RECOMBINANT JUST 2 OTHER WILL NOT BE VIABLE
55
RSULT OF PERICENTERIC HETEROZYGOTE CROSS OVER
2 NON RECOMBINANT BUT VIALBE 2 NON VAIVBLE NO DICENTRIC BRIDGE AND NO ACENTRIC
56
Balancer chromosomes
contains multiple inversions They are used in genetic analysis
57
TYPES OF TRNALSOCATION
RECIPROCAL AND NON RECIPROCAL
58
ROBERTSONIAN
2 ACROCENTRIC PUT THEIR Q TOPHATER DOWN SYNDROMM REDUCE THE NUMBER
59
SUMMERY OF THE INVERSION CROSS-OVER - PERICENTRIC
ALL NON RECOMBINANT 50 PERCENT VIABLE 1 INVERTED 1 NORMAL BUT NON RECOMBIANTN 1!!!
60
SUMMERY of the translocation in prophase 1 heterozygous- reciprocal
1- alternate produce all viable gamtest 20 adjucent 0 therfeore 50 percent only chnace vaibility 25 percent trnaslocated 25 percent normal
61
pseudolinkage of genes
can be seen in the translocation
62
tetravalent structure
structure can be seen in the translocation reciprocl during the prohpahse
63
semisterility
reciprocal heterozygote trnaslocation
64
acrocentric chromosome pairs
5 = 11,12,13,14,21,22 y crhomomse !
65
bioclimate zone in the italy
north: supratemprate mesotemprate mediterranean
66
.....appears to be strongly shaped by climatic factors
size and morphology
67
Bergmann’s rule
body weight/ mass vs environmental temperature relationship T decreases/ colder= mass of body / weight increase
68
Metabolic heat production
t strongly related to body mass
69
* Allen’s rule:
_ ecological rule _ body proportionality vs temperature relationship
70
pituitary gland
هیپوفیز
71
f low iodine intake
hypertrophy 200-300 million people are affected.adenomatous goiter.
72
goitrogenic.
prevent the incorporation and uptake of iodinebrassicaceae
73
* Lake Kivu in Rwanda goitre
t 54% in the population
74

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