Final W4 Flashcards

1
Q

There is a strong correlation between high levels of cholesterol in ___ and ___ disease. Cholesterol is a crucial component of ___ ___ and an important precursor to ___ hormones and __ ___. All ___ can synthesize cholesterol

A

blood, cardiovascular, cellular membranes, steroids, bile acids, cells

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2
Q

Stage one of cholesterol formation involves 2 molecules of ____ condensing to form _____. This product then condenses with a third molecule of acetyl-CoA to yield _____. This product is reduced to ____.

A

acetyl-CoA, acetoacetyl-CoA, HMG-CoA, mevalonate

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3
Q

In stage two of cholesterol formation, ___ ______ groups are transferred to mevalonate. The intermediate ________ _____ releases ____ and phosphate, producing an activated ____

A

3 phosphate, 3-phospho 5-pyrophosphomevalonate CO2, isoprene

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4
Q

In stage 3 of cholesterol formation, 2 activated isoprenes condense, forming __ ___ with __ carbons. This product ___ with another activated isoprene forming ___ ___ with ___ carbons. Two molecules of this product condense, forming ___ with ___ carbons

A

geranyl pyrophosphate, 10, condenses, farnesyl pyrophosphate, 15, squalene, 30

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5
Q

In the last stage of cholesterol formation __ ___ catalyzes the addition of one ___ atom from O2 to the end of squalene, forming an ____. ____ results in the formation of ___ which contains the __ rings characteristic of the steroid nucleus. Several additional reactions add and reposition ___ groups to form cholesterol.

A

squalene monooxygenase, oxygen, epoxide, cyclization, lanosterol, 4, methyl

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6
Q

Cholesterol can be formed into __ ___ which emulsify dietary fats, __ ___ which are hydrophobic molecules for lipoprotein transport, or ____ ___ such as testosterone and estradiol

A

bile salts, cholesterol esters, steroid hormones

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7
Q

hormone that promotes the activation of HMG-CoA reductase

A

insulin

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8
Q

Hormones that promote the inactivation of HMG-CoA reductase

A

glucagon, AMPK

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9
Q

___ ___ __ is the leading cause of death in developed countries. ___ are the most widely used drugs for lowering ___ cholesterol levels. They are ___ ___ of HMG-CoA reductase, resembling the substrate ____. The most widely used statin is _____.

A

coronary heart disease, statins, serum, competitive inhibitors, mevalonate, atorvastatin

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10
Q

Ketone bodies are produced in the ___ as an alternative fate for acetyl-CoA. ___ is produced in smaller quantities and exhaled. ___ and ______ are transported by blood to extrahepatic tissues. The ____ relies heavily on ketone bodies for fuel because fatty acids cannot cross the BBB

A

liver, acetone, acetoacetate, D-beta-hydroxybutyrate, brain

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11
Q

The synthesis of ketone bodies occurs in the __ __ of _____. First two molecules of acetyl-CoA condense to form _____. This condenses with another molecule of acetyl-CoA forming ___. This produced is cleaved to free ____ and ____. The latter is ___ reduced to ____ or ____ to acetone

A

mitochondrial matrix, acetoacetyl-CoA, HMG-CoA, acetyl-CoA, acetoacetate, reversibly, D-beta-hydroxybutyrate, decarboxylated

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12
Q

The breakdown of ketone bodies occurs in the mitochondria in __ ___. First, D-beta-hydroxybutyrate is oxidized to ____. This is then metabolized to ____. This produced is cleaved to 2 molecules of ___ which enters the citric acid cycle

A

extrahepatic, acetoacetate, acetoacetyl-CoA, acetyl-CoA

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13
Q

___ consumes oxaloacetate and slows citric acid cycle. The slowing of the citric acid cycle promotes __ ___ production. The release of ___ during the formation of acetoacetate enables the continued oxidation of __ ___.

A

gluconeogenesis, ketone body, CoA, fatty acids

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14
Q

During starvation, gluconeogenesis is __ to provide ___ to tissues such as the brain. This depletes citric acid cycle ___, resulting in ____ producing ketone bodies.

A

active, glucose, intermediates, acetyl-CoA

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15
Q

In people with diabetes, insufficient ___ prevents glucose uptake from the blood. Low glucose in cells stimulates ___ and ____, which depletes the citric acid cycle intermediates and produces ___ ___. Thus these individuals have a much higher concentration of ___ in the blood and urine.

A

insulin, beta-oxidation, gluconeogenesis, ketone bodies, acetoacetate

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16
Q

a condition in which the concentration of ketone bodies in the blood, tissues, and urine is abnormally high

A

ketosis

17
Q

dietary proteins are degraded to free __ ___ within the gastrointestinal tract. In the stomach, proteins stimulate the secretion of ____, which stimulates the secretion of ____ and _____. The latter is activated by autocatalysis at low _____. Active ___ cleaves polypeptides into peptides

A

amino acids, gastrin, HCl, pepsinogen, pH, pepsin

18
Q

Acidic stomach contents enter the small intestine and trigger the secretion of __, which stimulates the secretion of ___ to neutralize HCl. ____ is also secreted to stimulate release of several pancreatic ____ such as ____, ____ __ and ___. Active proteases cleave peptides into a mixture of free amino acids.

A

secretin, bicarbonate, cholescytokinin, proteases, trypsinogen, chymotrypsinogen, procarboxypeptidases A, B,

19
Q

an inactive precursor of an enzyme

A

zymogen

20
Q

In the small intestine, the free amino acids such as ___ and ____ are then transported into ___ cells, and transported to the __ via the __

A

di, tri-peptides, epithelial, liver, blood

21
Q

the dynamic regulation of a balanced functional proteome

A

proteostasis

22
Q

the degradation and resynthesis of proteins

A

protein turnover

23
Q

Ubiquitin is a ___ residue protein present in all ____ cells. This tags proteins for ____. The c-terminal ___ forms a ___ bond with ___ residues on target proteins

A

76, eukaryotic, destruction, glycine, covalent, lysine

24
Q

First the free ____ group of the c-terminal glycine residue in ubiquitin is bound to an ___ ___ enzyme through a ___ linkage. Then ubiquitin is transferred to an ______ _____ enzyme. An ______ ____ catalyzes transfer of ubiquitin from from E2 to the target protein

A

carboxyl, E1 activating, thioester, E2 conjugating, E3 ligase

25
Q

____ is 4 ubiquitin monomers linked by ___ bonds. Each bond is formed by the linkage of the ___ at the c-terminal to the _____ of a ___ residue. This is the primary signal for protein ____.

A

tetraubiquitin, isopeptide, carboxyl, lysine, degradation

26
Q

To a large extent, the half life of a cytoplasmic protein is determined by its ___ terminal residue. A yeast protein with a Met at its n-terminus has a half life of _____h. A yeast protein with an Arg at it’s n-terminus has a half life of ______. The N-terminal residue can be modified by ____ modifications

A

amino, <20, 3 minutes, posttranslational

27
Q

Ubiquitinated proteins are degraded by a large complex known as the ___ _____. It is made up of two ___ subunits and two ____ subunits. The general structure contains a ____ core with two regulatory particles at each end of the barrel.

A

26S proteasome, 19S, 20S, barrel-like

28
Q

The 19S regulatory particle has ___ subunits and forms a ___ at the end of the core particle. It recognizes ubiquitinated proteins and ___ and ___ them, then translocates the protein into the ___.

A

18, cap, deubiquinates, unfolds, core

29
Q

The 30S core particle consists of ___ rings arranged to form a barrel-like structure. The outer rings are formed with _____ ____ subunits, and the inner rings are formed from __ ___ subunits. ___ ___ subunits have protease activity

A

4, 7 alpha, 7 beta, 3 beta

30
Q

HPV expresses the ___ protein, which ___ and also binds ____, which is a tumor suppressor, and ____ a E3 ligase. The enhanced ubiquitination of p53 drives __ ___

A

E6, dimerizes, p53, E6AP, cancer progression

31
Q

Ubiquitinated proteins are processed to peptides within the ___ and ubiquitin is recycled. The peptide fragments are further digested to free __ _____ which can be used for ___. Amino groups can be excreted via the ___ ___, while carbon skeletons can be used for ___, ketone bodies, or __ __ synthesis

A

proteasome, amino acids, biosynthesis, urea cycle, gluconeogenesis, fatty acid