Investigation of tubulin aspects of cerebral protein 10-
By Mark McGary
Rather interesting observation details of the Plasmodium f. intersection via residue occur at the intersection cerebral protein 10 and plasmodium with outlier indications observed in ades e. at FKBP-type peptidyl-prolyl cis-trans isomerase [Aedes aegypti]
The structural component of the gene has rather interesting features, of which high acidic mole observation is a natural first inquiry. However, the high mole indicator at position 2 is useful to probe via selkov the causal nature of interior differentation in homo sapiens with the ceberal element premised to be directly attacked in the plasmodium presentation of case.
Of particular observation inference is a small, succinct residue group at :ESDNERDSDKESEDGEDEVSCETVK observed in human and the PREDICTED: regulator of microtubule dynamics protein 3-like [Loxodonta africana] 61.7 84.8 33% 5e-08 100% XP_003418704.1
It is with some rather extensive view within the larger tubulin assortment as regards residue that I can begin to make rather instant assessment of the high mole relief observed of prominence.
The renal tissue indication as well as the recent tubulin reversal within a oncology study deminstrates to the author a fundamental association of this gene residue as latent to the attack by pathway or schema…of several pathogen associations as well as observed oncological impacts.
Let us examine the repeat regionality of conservation in homo sapiens and hence move the the loxadonta for contrasting viewpoint.
1578 bp mRNA linear MAM 25-AUG-2011 DEFINITION PREDICTED: Loxodonta africana regulator of microtubule dynamics protein 3-like (LOC100662607), mRNA. ACCESSION XM_003418656 VERSION XM_003418656.1 GI:344293993 KEYWORDS RefSeq. SOURCE Loxodonta africana (African savanna elephant) ORGANISM Loxodonta africana
taxon:9606″ /tissue_type=”Brain” Protein 1..470 /product=”cerebral protein-10″ CDS 1..470 /gene=”hucep-10″ /coded_by=”AB000782.1:1..1413″ /inference=”non-experimental evidence, no additional details recorded” /note=”HUCEP-10″ ORIGIN 1 msrlgalgga raglglllgt aaglgflcll ysqrwkrtqr hgrsqslpns ldytqtsdpg 61 rhvmllravp ggagdasvlp slpregqekv ldrldfvlts lvalrrevee lrsslrglag 121 eivgevrchm eenqrvarrr rfpfvrersd stgsssvyft assgatftda eseggyttan 181 aesdnerdsd kesedgedev scetvkmgrk dsldleeeaa sgassaleag gssgledvlp 241 llqqadelhr gdeqgkregf qlllnnklvy gsrqdflwrl araysdmcel teevsekksy 301 aldgkeeaea alekgdesad chlwyavlcg qlaehesiqr riqsgfsfke hvdkaialqp 361 enpmahfllg rwcyqvshls wlekktatal lesplsatve dalqsflkae elqpgvskag 421 rvyiskcyre lgknsearww mklalelpdv tkedlaiqkd leelevilrd //
Recently, I have been rather interested in direct conserved mutation in neonate as pathogenesis, and this combined locus seems to rather make sense as an avenue to discern mutation causality.
I suspect the cocci residues are involved, but unraveling the avenues by selkov should present the most factual intersections to be observed.
Why? Because the Selkov determinants of high mole indication, are now oraganized into single endpoint indicator. This method is leading to topological model of gene signal. *ie. on – off.
mutational scarring of needed conservation for normal neonatal development seems to be within reach, and of course presents the implication of develomental methods by conformational relief as a research viewpoint.
The tubulin aspect seems succinct via observational intersection in larger cranial observation seen in loxodanta and homo sapiens.
The author simply needs to take advantage of this implied organizational resource to the sets of protein residue in view as pathogenicity…..and aberant conservation to presentation in case.