SLC24a5. Meseret Was Bored Last Night. Here! Perk Up!

SLC24a5.  hocked: hocked: hocked: hocked:
::rofl:: ::rofl:: ::rofl:: ::rofl::
::rofl:: ::rofl:: ::rofl:: ::rofl::

they found the gene for whiteness and hit all the Coonians for a loop.

Polygenesis...smollygenis. Monogenesis!

slow me! 

deh found this some time ago and only yesterday an aquaintance mentioned it to me..I came to know of it. a derivative of the genome project.

ALL THE ARGUMENT DONE!

http://en.wikipedia.org/wiki/SLC24A5





SLC24A5
From Wikipedia, the free encyclopedia
Solute carrier family 24, member 5
Identifiers
Symbols  SLC24A5; JSX; NCKX5; SHEP4
External IDs  OMIM: 609802 MGI: 2677271 HomoloGene: 18400 GeneCards: SLC24A5 Gene
[show]Gene Ontology
Orthologs
Species  Human  Mouse 
Entrez  283652  317750 
Ensembl  ENSG00000188467  ENSMUSG00000035183 
UniProt  Q71RS6  Q8C261 
RefSeq (mRNA)  NM_205850.2  NM_175034.3 
RefSeq (protein)  NP_995322.1  NP_778199.2 
Location (UCSC)  Chr 15:
48.41 – 48.43 Mb  Chr 2:
124.89 – 124.91 Mb 
PubMed search  [1]  [2] 
This box: view talk edit
Sodium/potassium/calcium exchanger 5 (NCKX5) also known as solute carrier family 24 member 5 (SLC24A5) is a protein that in humans is encoded by the SLC24A5 gene that has a major influence on natural skin colour variation.[1] The NCKX5 protein is a member of the potassium-dependent sodium/calcium exchanger family. Sequence variation in the SLC24A5 gene, particularly a non-synomyous SNP changing the amino acid at position 111 in NCKX5 from alanine to threonine, has been associated with differences in skin pigmentation.[2]
Contents  [hide]
1 Gene
2 Protein
3 Effect on skin color
4 See also
5 References
6 Further reading
7 External links
[edit]Gene


The SLC24A5 gene, in humans, is located on the long (q) arm of chromosome 15 on position 21.1, from base pair 46,200,461 to base pair 46,221,881.[1]
[edit]Protein


NCKX5 is 43 kDa protein that is partially localized to the trans-Golgi network in melanocytes. Removal of the NCKX5 protein disrupts melanogenesis in human and mouse melanocytes, causing a significant reduction in melanin pigment production. Site-directed mutagenesis corresponding to a non-synonymous single nucleotide polymorphism in SLC24A5 alters a residue in NCKX5 (A111T) that is important for NCKX5 sodium-calcium exchanger activity.[2]
[edit]Effect on skin color


SLC24A5 appears to have played a key role in the evolution of light skin in humans of European ancestry. The gene's function in pigmentation was discovered in zebrafish as a result of the positional cloning of the gene responsible for the "golden" variety of this common pet store fish. In this work, cancer geneticist Keith Cheng used electron microscopy to probe the cellular mechanism underlying the lighter color of golden zebrafish, and noted a striking similarity between the changes of melanocytes (pigment cells) in those lighter-skinned fish and lighter-skinned humans (in particular, Europeans). This led Cheng to ask his Pennsylvania State University colleague, anthropologist Mark D. Shriver, whether he had human DNA linked to skin color measurements. Shriver, who collaborates internationally to study the basis of variation in human skin color and other features in human populations, pointed to the then-new International HapMap Project database of genetic variation in human populations, and found that the gene has a single "coding" polymorphism - one that changes an amino acid. The two primary alleles differ in only one nucleotide, changing the 111th amino acid from alanine to threonine, abbreviated "A111T".[1][3][4]
The threonine allele was present in 98.7 to 100% among several European samples, while the alanine form was found in 93 to 100% of samples of Africans, East Asians and Indigenous Americans. The variation is a SNP polymorphism rs1426654, which had been previously shown to be second among 3011 tabulated SNPs ranked as ancestry-informative markers. Collaborator Victor Canfield plotted the human data to estimate that this single change in SLC24A5 explains between 25 and 38% of the difference in skin melanin index between peoples of West African vs. European Ancestry.
The discovery of this gene has interesting social implications because the "derived" European allele was derived by mutation from the ancestral gene sequence. As noted by Penn State's Victor Canfield, the ancestral alanine is conserved in all vertebrates sequenced to date, mutant only in the European allele, but only rarely in West African or East Asian (primarily Chinese, Japanese and Korean) populations (presumably by admixture). Furthermore, the European mutation is associated with the largest region of diminished genetic variation in the CEU HapMap population, suggesting the possibility that the A111T mutation may be the subject of the single largest degree of selection in human populations of European ancestry. Selection for the derived allele is based on the need for sunlight to produce the essential nutrient, vitamin D. In northerly latitudes, there is less sun, greater requirement for body coverage due to colder climate, and frequently, diets poor in vitamin D, making lighter skin necessary for survival. Tests for this variation has obvious application to forensic science.
It has been estimated that the threonine allele became predominant among Europeans 5,300 to 6,000 years ago [5].

ketchim...food fuh yu.  eat up!


I mean..eat yuh lentils ::rofl:: ::rofl:: ::rofl:: ::rofl::

http://en.wikipedia.org/wiki/Threonine

SCL have to use a lotta SLC  ....to get fair skin  ::redcard::

                         

put it in a nutshell for me Maps, i busy busy busy .. no time to read.

[quote author=Meseret link=topic=68984.msg430450#msg430450 date=1343237578]
put it in a nutshell for me Maps, i busy busy busy .. no time to read.
[/quote]


the gene for whiteness has been found

SLC24a5..a human gene responsible for skin pigmentation, recently discovered, proves finally, conclusively, that the origin of white skin, is from genetic mutation of  existing original human physiology that pre-dates white people...and not a separate evolution on their own


separate white evolution is posed by a theory  known as poly-genesis..which claims that at separate locations humans evolved  into the known ethnicities we know currently..as opposed to mono-genesis  that has established that humans evolved in africa and spread throughout the world, changing in response to the varying environmental challenges in the nooks and crannies of the world encountered and successfully colonized by our species.


the most famous name behind poly-genesis is Carlton Coon .  he is now defeated comprehensively, his theory debunked.


but what the racist are doing is to shift their ground a little, by posing that the original  aurignacian settler of europe, who deposed or succeeded neanderthal are middle eastern types or browns from India..or even neanderthal himself....that they are the ones who imparted the threonine the basic allele in the process of the change from blac to white skin.


the aurignacians were black people out of africa and nowhere else.  at the earliest times middle eastern types did not exist.  they are a product of mixing around the meditarrenean area of confluence.


white people..some at least do not want to accept the facts of their origins.  at least one part of the argument is done anyway

the links above describes the gene and much of what is known about it, its location in the body etc