Hello March. Hello.
Mar. 1st, 2012 12:21 am![[personal profile]](https://www.dreamwidth.org/img/silk/identity/user.png){kind=small}
coolerthanthouHello March. I hope you will treat me well. (:
Carnitine Shuttle
Used as fatty acyl CoA is bulky and polar and cannot get across the inner mitochondrial matrix and must be carried by a carrier - Carnitine.
Carnitine combines with fatty acyl CoA to form Acyl Carnitine, releasing CoA. Acyl Carnitine can now be transferred from the cytosol into the mitochondrial matrix across the inner mitochondrial matrix.
Acyl Carnitine, now in the mitochondrial matrix recombines with CoA, to form fatty acyl CoA. Carnitine is released.
Carnitine is recycled back into the cytosol to shuttle another fatty acid.
This shuttle is used as to have Beta-oxidation to take place, the fatty acids need to be activated and the activation takes place in the cytosol while beta-oxidation takes place in the mitochondrial matrix.
The Acyl carrier is CoA.
Citrate Shuttle.
To have fatty acid synthesis to take place, Acetyl CoA, which is synthesized in the mitochondrial matrix needs to be transported to the cytosol for fatty acid synthesis to take place.
Acetyl CoA binds with oxaloacetate to form citric acid in order to be transported into the cytosol with the help of citrate synthase. Once citric acid is in mitochondrial matrix, citric acid is being cleaved by citrate lyase to Acetyl CoA and Oxaloacetate.
Acetyl CoA is then catabolized by Acetyl CoA carboxylase to get Malonyl CoA.
Malonyl CoA is catabolized by a multienzyme complex, the fatty acid synthase to fatty acids.
Protein Synthesis
Takes place in 2 stages:
1. Transcription
2. Translation
1. Transcription = genetic message is copied from DNA to mRNA in the nucleus.
Genetic code for protein synthesis is in the DNA but they are too large to pass through the nuclear membranes into the cytosol where proteins are synthesized and hence the messenger RNA molecules carry genetic information from nucleus to the cytosol.
DNA is tightly wound together in a super coil. It uncoils itself with the help of DNA helicase and gyrase. A single strand of protein binds to the unpaired strand to prevent recoiling/reformation of the double helix.
Transcription starts as RNA polymerase I binds to the promoter at the beginning of the gene, initiating formation of complimentary RNA strand.
When RNA polymerase I arrives at the end of the gene, it receives a 'stop' signal and disengages from DNA. The newly assembled RNA strand is processed before exiting the nucleus. (DNA strand used = sense strand)
Transcribed gene is made up of 2 segments, exons and introns. mRNA undergoes splicing to remove introns to make it 75-90% shorter, to allow it to pass through the nuclear pores.
2. Translation
Once mRNA is transcribed and spliced, it moves through the pores into the cytoplasm where it binds with a ribosome. The ribosome contains enzymes required for the translation of mRNA's coded message into a protein.
3 steps: Initiation, elongation and termination.
Initiation:
mRNA binds to small ribosomal subunits, which binds to the large ribosomal subunit to make a functional ribosome.
Initiator tRNA carrying the first amino acid fits into the P site, its anticodon pairing with the start codon on the mRNA.
Elongation:
The next tRNA carrying the second amino acid fits into the A site, its anticodon pairing with the next codon on the mRNA. A peptide bond is formed between the 2 amino acids, creating a dipeptide. The initiator tRNA detaches itself from the P site. The secon tRNA is translocated to the P sites, leaving the A site free for the next tRNA.
The process is repeated: A peptide bond is formed with the new amino acid unit, the tRNA detached itself from the P site, remaining unit is translocated to leave the A site free for the next attachment.
Termination:
Begins when ribosome reaches a stop codon on the mRNA. The polypeptide is released while the other components dissociate.
Polypeptide bond is assembled exactly to the directions.
Glycogenesis
Glucose -> Glucose 6-phosphate -> Glucose 1-phosphate + Uridine triphosphate - (- PPi)> Uridine diphosphate glucose -glycogen synthase> Existing glycogen chains.
- Stimulated by high levels of insulin, takes place in all animal tissues esp. in liver and in skeletal muscles.
Glycogenolysis
Glycogen (stores in the liver) -glycogen phosphorylase> Glucose 1-phosphate -phophoglucomutase> Glucose 6-phosphate -glucose 6-phosphatase> Glucose -GluT2> Into the blood.
Only liver glycogen are used in glycogenolysis for energy as muscles does not have the enzyme Glucose 6-phosphatase .
Gluconeogenesis
= Production of glucose from non-carbohydrate sources such as Lactate, Glycerol, Amino Acids and Pyruvate as sources of carbon for the pathway.
Takes place in the liver and in some extent, kidneys. Takes place when blood glucose is low and carbohydrates is not available, hormone cortisol from adrenal cortex diverts some amino acids from body cells to liver and converts them into glucose. Thyroxine may also divert triglycerides from adipose tissues to the liver where the glycerol portion is converted to glucose. Pyruvic/Lactic acid is converted to glucose and recycled back to the muscle glycogen through Cori Cycle.
Prevents hypoglycemia, preventing neonatal deaths by supplying continuous supply of glucose as metabolic fuel.
Cori Cycle = Glycolysis + Gluconeogenesis.
HMP Shunt = Oxidative phase + Non-oxidative phase.
Oxidative phase: Glucose 6-phosphate -> Pentose Phosphate. NADPH generated.
Non-oxidative phase: Pentose Phosphate -> Glucose 6-phosphate.
Takes place mainly in the liver, some extent, kidney, mysckes and brain.
NADPH generated is especially important for RBCs for the supply of glutathione generated by NADPH to prevent oxidative damages. It is also needed for the synthesis of nucleic acids and also for biosynthetic reactions like fatty acid, cholesterol and steroid hormone synthesis.
ETC
The final step in oxidation of metabolic fuel. ETC oxidizes NADH to NAD+, FADH2 to FAD. =
Electrons are transferred from NADH & FADH2 through a series of electron carriers to Oxygen, forming metabolic water.
ETC is the final common pathway in aerobic cells by which electrons derived from various substrates (CHOs, proteins, lipids, alcohols) are transferred to Oxygen.
Takes place in IMM.
Involves 4 lipid protein complexes 1 to 4 and four types of electrons carrying molecules: Flavin Mononucleotide, Iron-sulfur proteins, ubiquinone, cytochromes.
Each of the electron carriers are first reduced then oxidized as electrons and transported through the chains to oxygen (electron acceptor).
Oxidized NAD+/FAD generated are re-channeled to various metabolic pathways while Oxygen, the ultimate electron acceptor is being reduced to metabolic water.
There are 2 entry points into ETC - One for electrons from NADH, one for electrons from FADH2. As electrons move down the complexes, the complexes have higher and higher affinity for electrons, making them easier to reduce. As FADH2 is a less powerful electron donor than NADH, it jumps to complex 2, with less reduction potential. The weak FADH2 jumps to the second complex where proteins are easier to reduce otherwise it will not have enough potential to make it all the way through ETC to oxygen.
I'm sorry if you've clicked on the cut to find out what it is. I am really just very worried about my biochemistry paper later on.
The last paper. 2 hours worth. I think I can do this. I think.
Tillagain.
Carnitine Shuttle
Used as fatty acyl CoA is bulky and polar and cannot get across the inner mitochondrial matrix and must be carried by a carrier - Carnitine.
Carnitine combines with fatty acyl CoA to form Acyl Carnitine, releasing CoA. Acyl Carnitine can now be transferred from the cytosol into the mitochondrial matrix across the inner mitochondrial matrix.
Acyl Carnitine, now in the mitochondrial matrix recombines with CoA, to form fatty acyl CoA. Carnitine is released.
Carnitine is recycled back into the cytosol to shuttle another fatty acid.
This shuttle is used as to have Beta-oxidation to take place, the fatty acids need to be activated and the activation takes place in the cytosol while beta-oxidation takes place in the mitochondrial matrix.
The Acyl carrier is CoA.
Citrate Shuttle.
To have fatty acid synthesis to take place, Acetyl CoA, which is synthesized in the mitochondrial matrix needs to be transported to the cytosol for fatty acid synthesis to take place.
Acetyl CoA binds with oxaloacetate to form citric acid in order to be transported into the cytosol with the help of citrate synthase. Once citric acid is in mitochondrial matrix, citric acid is being cleaved by citrate lyase to Acetyl CoA and Oxaloacetate.
Acetyl CoA is then catabolized by Acetyl CoA carboxylase to get Malonyl CoA.
Malonyl CoA is catabolized by a multienzyme complex, the fatty acid synthase to fatty acids.
Protein Synthesis
Takes place in 2 stages:
1. Transcription
2. Translation
1. Transcription = genetic message is copied from DNA to mRNA in the nucleus.
Genetic code for protein synthesis is in the DNA but they are too large to pass through the nuclear membranes into the cytosol where proteins are synthesized and hence the messenger RNA molecules carry genetic information from nucleus to the cytosol.
DNA is tightly wound together in a super coil. It uncoils itself with the help of DNA helicase and gyrase. A single strand of protein binds to the unpaired strand to prevent recoiling/reformation of the double helix.
Transcription starts as RNA polymerase I binds to the promoter at the beginning of the gene, initiating formation of complimentary RNA strand.
When RNA polymerase I arrives at the end of the gene, it receives a 'stop' signal and disengages from DNA. The newly assembled RNA strand is processed before exiting the nucleus. (DNA strand used = sense strand)
Transcribed gene is made up of 2 segments, exons and introns. mRNA undergoes splicing to remove introns to make it 75-90% shorter, to allow it to pass through the nuclear pores.
2. Translation
Once mRNA is transcribed and spliced, it moves through the pores into the cytoplasm where it binds with a ribosome. The ribosome contains enzymes required for the translation of mRNA's coded message into a protein.
3 steps: Initiation, elongation and termination.
Initiation:
mRNA binds to small ribosomal subunits, which binds to the large ribosomal subunit to make a functional ribosome.
Initiator tRNA carrying the first amino acid fits into the P site, its anticodon pairing with the start codon on the mRNA.
Elongation:
The next tRNA carrying the second amino acid fits into the A site, its anticodon pairing with the next codon on the mRNA. A peptide bond is formed between the 2 amino acids, creating a dipeptide. The initiator tRNA detaches itself from the P site. The secon tRNA is translocated to the P sites, leaving the A site free for the next tRNA.
The process is repeated: A peptide bond is formed with the new amino acid unit, the tRNA detached itself from the P site, remaining unit is translocated to leave the A site free for the next attachment.
Termination:
Begins when ribosome reaches a stop codon on the mRNA. The polypeptide is released while the other components dissociate.
Polypeptide bond is assembled exactly to the directions.
Glycogenesis
Glucose -> Glucose 6-phosphate -> Glucose 1-phosphate + Uridine triphosphate - (- PPi)> Uridine diphosphate glucose -glycogen synthase> Existing glycogen chains.
- Stimulated by high levels of insulin, takes place in all animal tissues esp. in liver and in skeletal muscles.
Glycogenolysis
Glycogen (stores in the liver) -glycogen phosphorylase> Glucose 1-phosphate -phophoglucomutase> Glucose 6-phosphate -glucose 6-phosphatase> Glucose -GluT2> Into the blood.
Only liver glycogen are used in glycogenolysis for energy as muscles does not have the enzyme Glucose 6-phosphatase .
Gluconeogenesis
= Production of glucose from non-carbohydrate sources such as Lactate, Glycerol, Amino Acids and Pyruvate as sources of carbon for the pathway.
Takes place in the liver and in some extent, kidneys. Takes place when blood glucose is low and carbohydrates is not available, hormone cortisol from adrenal cortex diverts some amino acids from body cells to liver and converts them into glucose. Thyroxine may also divert triglycerides from adipose tissues to the liver where the glycerol portion is converted to glucose. Pyruvic/Lactic acid is converted to glucose and recycled back to the muscle glycogen through Cori Cycle.
Prevents hypoglycemia, preventing neonatal deaths by supplying continuous supply of glucose as metabolic fuel.
Cori Cycle = Glycolysis + Gluconeogenesis.
HMP Shunt = Oxidative phase + Non-oxidative phase.
Oxidative phase: Glucose 6-phosphate -> Pentose Phosphate. NADPH generated.
Non-oxidative phase: Pentose Phosphate -> Glucose 6-phosphate.
Takes place mainly in the liver, some extent, kidney, mysckes and brain.
NADPH generated is especially important for RBCs for the supply of glutathione generated by NADPH to prevent oxidative damages. It is also needed for the synthesis of nucleic acids and also for biosynthetic reactions like fatty acid, cholesterol and steroid hormone synthesis.
ETC
The final step in oxidation of metabolic fuel. ETC oxidizes NADH to NAD+, FADH2 to FAD. =
Electrons are transferred from NADH & FADH2 through a series of electron carriers to Oxygen, forming metabolic water.
ETC is the final common pathway in aerobic cells by which electrons derived from various substrates (CHOs, proteins, lipids, alcohols) are transferred to Oxygen.
Takes place in IMM.
Involves 4 lipid protein complexes 1 to 4 and four types of electrons carrying molecules: Flavin Mononucleotide, Iron-sulfur proteins, ubiquinone, cytochromes.
Each of the electron carriers are first reduced then oxidized as electrons and transported through the chains to oxygen (electron acceptor).
Oxidized NAD+/FAD generated are re-channeled to various metabolic pathways while Oxygen, the ultimate electron acceptor is being reduced to metabolic water.
There are 2 entry points into ETC - One for electrons from NADH, one for electrons from FADH2. As electrons move down the complexes, the complexes have higher and higher affinity for electrons, making them easier to reduce. As FADH2 is a less powerful electron donor than NADH, it jumps to complex 2, with less reduction potential. The weak FADH2 jumps to the second complex where proteins are easier to reduce otherwise it will not have enough potential to make it all the way through ETC to oxygen.
I'm sorry if you've clicked on the cut to find out what it is. I am really just very worried about my biochemistry paper later on.
The last paper. 2 hours worth. I think I can do this. I think.
Tillagain.
