It looks like you're using an Ad Blocker.
Please white-list or disable AboveTopSecret.com in your ad-blocking tool.
Thank you.
Some features of ATS will be disabled while you continue to use an ad-blocker.
Apparently I read far more of it than you did because it discusses specifically how a new protein was created that confers beneficial immunities against a specific group of viruses.
originally posted by: neoholographic
a reply to: Noinden
Again, you didn't provide any evidence. You couldn't articulate a response so you posted 3 links and said go fish.
Just imagine if every thread on ATS consisted of just links with no commentary or context LOL.
YOU CAN'T BE SERIOUS!
If you can't articulate a response then you should find a forum where people just post links without commentary or context.
originally posted by: neoholographic
a reply to: Noinden
Again, you didn't provide any evidence. You couldn't articulate a response so you posted 3 links and said go fish.
Just imagine if every thread on ATS consisted of just links with no commentary or context LOL.
YOU CAN'T BE SERIOUS!
If you can't articulate a response then you should find a forum where people just post links without commentary or context.
originally posted by: neoholographic
a reply to: Noinden
Again, you didn't provide any evidence. You couldn't articulate a response so you posted 3 links and said go fish.
Just imagine if every thread on ATS consisted of just links with no commentary or context LOL.
YOU CAN'T BE SERIOUS!
If you can't articulate a response then you should find a forum where people just post links without commentary or context.
If evolution is the change in DNA.
then every viral infection is an evolution,
every mitotic division is an evolution (telomeres are lost, thus changing DNA composition),
and meiosis must then be evolution due to crossing over of the genetic coding.
Surely, these are not examples of evolution, try again with the definition.
originally posted by: Noinden
a reply to: Phantom423
Yep. @neoholographic
READ
THE
PAPERS
They are not that esoteric. I indeed made sure I left the really dense Bioinformatic ones out
originally posted by: neoholographic
a reply to: peter vlar
The combination produces a single protein capable of blocking infection by viruses closely related to HIV.
It never said anything was created it said THE COMBINATION PRODUCED. There was no regulatory change or any sequence change in the regulation of expression of TRIM5-CrypA that CREATED a new function.
Random mutation don't bestow meaning or function on a sequence of DNA letters that regulate expression.
Thus, the mutation, which interferes with expression of the normal TRIM5α protein, instead contributes to expression of a novel protein.
We have previously reported that the TRIM5 coding sequence of old world monkeys is highly polymorphic [7]. In the course of genotyping the TRIM5 locus in a colony of captive bred rhesus macaques, we identified a single-nucleotide polymorphism in the terminal nucleotide of intron 6 (Figure 1). The SNP is the result of a G-to-T substitution that alters the canonical 3′ splice acceptor site (AG to AU) immediately upstream of exon 7. Initial sequence data revealed the presence of this mutation in 2 of 8 animals, including one homozygote (T/T) and one heterozygote (G/T). The cis-acting AG element at the end of introns is a highly conserved feature of 3′ splice sites, and the presence of such a mutation is predicted to interfere with mRNA splicing.
The predicted proteins encoded by the TRIM5-CypA chimeric transcripts of Asian macaques and South American owl monkeys are remarkably similar (Figure 3). However, unlike owl monkey TRIMCyp, macaque TRIM5-CypA did not block infection by HIV-1. There are multiple nonsynonymous differences between the two proteins, including differences in both the TRIM5 and CypA related domains. In addition, relative to owl monkey TRIMCyp, the macaque variants are missing 9 amino acids corresponding to exon-7 of TRIM5 and perhaps these residues are critical for function of the chimeric protein. It has previously been shown that artificial fusions between CypA and the RBCC domain of rhesus TRIM5α can restrict HIV-1 [15],[34]. Therefore, the functional differences between owl monkey TRIMCyp and macaque TRIM5-CypA (as measured against HIV-1) may instead be due either to differences in the CypA domains, the missing sequences corresponding to exon-7 [35], or both. Some or all of the amino-acid differences, as well as the observed differential restriction of HIV-1, may reflect differences between the natural agents of selection encountered by owl monkey TRIMCyp and macaque TRIM5-CypA during the evolution of each lineage.