Definition of created kind!

Hi, Im new and a creationist. I looked back at messages 46 to 60 where a creationist and an evolutionists discussed created kinds. I didnt have more energy to read much further.
But a good definition of microevolution and impossible macroevolution would be this:Every individuals in a created kind have the same protein transduction pathways, one spieces might have LOST a protein transduction pathway or the protein transduction pathways might be linked to each other by mutations. (Testosterone give rise to a mane in lions but not to other cats.)That is for example protein chains producing different cells that have even more different protein system.There might be arised dubble genes or one or a few extra proteins acting together with these ordinary vitally important systems. An extra protein change the regulation. That protein might cause a shortnosed dog like a pekingese, like a cat.But the cats have a more flexible spine. This might be due - (I dont know. But I would like to know) - to many different proteins acting together. If the cats have this protein system and the dogs doesnt, it shows 2 different kinds.

Do so! Ill start discussing from there!

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Originally posted by Zhimbo:

1. Are you suggesting a possible starting point for a defintion of "kind", or are you arguing that "different protein transduction pathways" could NOT arise via evolution. Or both?

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Both! The definition of created kind refers to both microevolution and macroevolution.

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Originally posted by Zhimbo:

2. You seem to allow that proteins can double (rather, the gene that codes a protein can have another copy in the genome), and that proteins can change due to mutation. If you allow these, what exactly is left for a new "protein transduction pathway"? Those two things can create two genes that code for two different proteins. What's missing?

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Those accumulating new proteins should start interact with one another or interact with already existing proteins. The question is how many new proteins can interact with eachother before they stop vitally important Signal Transduction Pathways (STP). So how big could a new STP be at maximum. 3-5 new proteins, I dont know. And every mutation doesnt produce new proteins.
So whats missing is a whole set of new proteins, sugars that interact without breaking a vitally important STP.

Ofcourse! Only A, T and Z are welcome here. Hehe!Can you show me those interesting refs?

I meant Signal Transduction Pathway (STP). Someone corrected me about this. So I use Signal and not protein.

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Originally posted by Zhimbo:

2. Second, I'm not sure why any new protein would necessarily "break" an exisiting transduction pathway (of either sort), or why 3-5 new proteins suddenly would, or whatever. As long as the original proteins were also being made, I don't see any necessary problem.

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Unfortunately, I don't think you're suceeding in creating a workable definition/standard for "created kind", although I'm still seeing where you're going. It seems more like you're just saying you don't see how systems of proteins could form. I don't see that you've created any barrier, though. You talk about new proteins breaking old pathways, but I don't see how this is inevitable.

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We should consider a typical STP+extracellular signals. Well, maybe I should use the word protein systems. Because STP only occurs within a cell. I focusing on the total intelligent signal from molecule to molecule.Ok, we have Protein System A: signal molecule A, receptor A, the transduction proteins within a cell, reprossors and inducers. The more molecules and bigger reaction sites the more complex it is.Protein System B: signal molecule B, receptor B, the transduction proteins within a cell, reprossors and inducers. The more molecules and bigger reaction sites the more complex it is.Protein System C: signal molecule C, receptor C, the transduction proteins within a cell, reprossors and inducers. The more molecules and bigger reaction sites the more complex it is.If a new protein in celltype A arise would it immediately cause
any trouble by acting with those transduction proteins. If it would be good it would maybe make the transduction more efficient. A protein is added to STP A. But what would next protein in celltype A do. If that also is good it would make the STP a little more even efficient. They dont produce any new protein system, they are just being added to the existing one. But soon enought bad mutations occur and destroy the whole package of accumulated proteins.And if celltype A produce a hormone that trigger signal molecule C its good. And then celltype B produce another hormone that also might help protein system C. The third hormone from celltype B produce a protein that destroy protein system C totally. The organism die.If a new protein system is going to be produced the new proteins must NEVER EVER disturb a vitally important system. So how the questions is: Will these new proteins react only themselves and how many new proteins until the organism die.

Dont worry Jeff.Maybe we havnt FOUND a protein systeme (PS)=(STP + Extracellular signals)=(STP + ES) yet that differ us from chimps.But the clear anatomical differences indicate that there are some particular different PS:s that differ us.

Thats just because the dangerous organism cant bind. After a few mutations things are going worse.

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Originally posted by Zhimbo:
There are clear anatomical differences between lions and pet cats, yet creationists generally consider them the same kind.

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Those anotomical differeneces arent bigger than between us and chimps, are they.

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Originally posted by Zhimbo:
New proteins can interact with any number of systems, or none. I can't figure out why you assume at some point the influence *must* be destructive. You ask "how many new proteins until the organism die." I say - not necessarily ever. There's no necessary limit to the number of protein changes. Sure, at some point some individual will have a bad mutation, but chances are it won't get passed on, assuming it's really bad. That's selection at work.

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A frame shift mutation often produce totally different proteins, with lots of possibilities to bind anywhere by chance. If these just leak out/heap up in the blood or within a cell I just cant imagine that they build up a new system themselves and none of them not at any time bind dangerously to a vitally important system. The only good thing they can do is to regulate ordinary protein systems to work more or less efficient.
Bad or good could also be whether they bind to an organism or not. Its bad to bind to a malaria-parasite. For a leguminous plant its good to take contact with Rhizobium bacteria.

InvitationIve started a msn-group about this subject: Created kindsPlease join! http://groups.msn.com/CreatedkindsZauruz

Tranquility and Brad. Im a biology student.What do you think of my definition when I started this topic? Is there a certain lack?"How many new frameshift mutation proteins and new point mutation proteins can be accumulated inside cells or in the interstitial fluid until the organism die. And when they accumulate, how few and short protein systems do they build up max.Tranquility: You are talking about protein folding. Ok, so when a protein with a certain folding will turn into another folding its straight/denatueted. But doesnt these proteins also have active binding sites, so they could bind dangerously to a system. Are all denatueted proteins dangerous? Hence your definition of created kinds.

What i get from the information of protein folding on internet, is that point mutations often radically change the protein. Couldnt thus just a point mutation make a totally new alfa-helix instead of a beta-sheat? A new folding thus or are point mutations in most cases causing denatuation.I still think that the certain binding sites of proteins and sugars in combination with different ion-concentration is the most important to focus at.

Evolutionists believe that new proteins after new proteins make it more complex. These mutations are thought be be good all the way up to the new systems, besides other individuals, who have bad mutations spoiling it all. And thats where we have to hit them.
I didnt mean that you were WRONG with the protein foldings. I was interested in it. But first I thought that unfolded proteins might do kind of the same things as a folded protein. For example regulate a system a little. But now I just learned that they aggregate!!We could combine this to: "How many new folded proteins (not new foldings) can accumulate until its lethal to have any new folded protein". If an unfolded one appear, or if any negative mutation appear, then the organism die. And different foldings as well as different embryology is thus a sign of different created kinds.

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Originally posted by Tranquility Base:

Can you briefly and clearly explain your point about 'binding sites of proteins and sugars in combination with different ion-concentration'.

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I meant that a protein could be active or inactive whether its bound to an ion or not. I the muscle-cell: When a Ca-ion hit Troponin, troponin change it form so tropomyosin draw back and expose actin binding sites to myosin heads.

Ok, take your time!