The codon is a set of 3 nucleotides that can be read to convey a message in your DNA. It can be a code saying to "start" the process of protein synthesis, or "stop" it, or to encode for an amino acid - the building blocks of proteins.
<span>The DNA is read, and proteins are made by DNA Polymerase (simple version here, it is more complicated, but this is the gist of it) travelling down the DNA. As it travels, it reads the nucleotides and builds a chain of amino acids, that corresponds to the information gleaned from the DNA. </span>
<span>So, the codon is only on one side of the DNA, and there are 2 sides. In order to be able to keep the DNA safe, and package it well (and loads of other reasons ) there is a complimentary strand. The nucleotides that make up DNA are A, T, C, and G. A links to T and C to G, and vice versa. </span>
So if your DNA strand's codons read "AAG AGG TCA"
Then the complimentary strand will read "TTC TCC AGT" the three codons on the complimentary strand ARE THE ANTICODONS of the codons on the strand being read (aka "expressed").
<span>So a codon and an anti codon are made of the same things, it just is a matter of which is being actively expressed. Now, this gets insanely complicated when you learn more about reading frames! Not only are there those codons, but if you shift and start reading the "code" either one nucleotide earlier or later, it completely changes the message.</span>
Https://www.nature.com/scitable/topicpage/the-information-in-dna-determines-cellular-function-652322...
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Numerous degenerative neurological conditions, most notably Parkinson's disease, have been linked to an excessive buildup of alpha synuclein (a-syn) in the brain. Intraneuronal inclusions, often known as Lewy bodies, are neuropathological characteristics seen in Parkinson's disease, Lewy body dementia, and other synucleopathies. The aggregation of a-syn is their main structural component. A-syn accumulation, aggregation, and ensuing Lewy body formation can be attributed to a variety of biological processes. These include genetic changes in parkin, synuclein, or the deubiquitinating enzyme ubiquitin C-terminal hydrolase (UCH-L1), which results in less efficient removal of a-syn via the ubiquitin proteasomal pathway (UPP). Additionally, environmental variables and an age-related decline in antioxidant defense mechanisms that heighten oxidative stress and can have an impact on the formation or clearance of a-syn are intracellular insults.
We focused on changes in the aggregation and clearance of a-syn as impacted by the UPP and the oxidative stress pathways in our dynamic models of a-syn processing in both normal and various disease states. A free radical profile similar to that observed in vivo after exposure to the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine is produced during simulation of enhanced oxidative stress (MPTP). To replicate the kinetics of a-syn that correlates to the neuropathology reported for the sporadic and hereditary types of Parkinson's disease, different model parameters of oxidative stress, UPP failure, or both routes are used. With the use of this in silico model, it is possible to evaluate the kinetics of pathway elements and more accurately identify and validate key pharmaceutical targets.
Learn more about Parkinson's disease brainly.com/question/28169444
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Hello there.:D
Which is an adaptation?A. A dog is trained to catch a ball.
B. A person learns how to do math.
C. A rabbit has fur that blends in with snow
D. A bird breaks its wing in an accident.
C. A rabbit has fur that blends in with snow
