PNC-27 valde iaculis anti-cancer peptide.
Vinculum inter dapibus suppressoris inhibet p53 et regulator ejus negans HDM-2.
HDM-2, an E3 ubiquitin ligase, ubiquitin mediatam degradationem promovet ad ligationem p53.
Cancer cellulae sic auctum inhibitionis et normalem consociatam evadunt apoptosis circuitus.
PNC-27 mimi nuclei segmenti p53 (amino acida 12-26) ipsum, preferentially binding hoc HDM-II ".
Egregie, PNC-XXVII segmentum singulare habet dives in . basic amino acida, adiuvando in eo quod nimis desideratur membranarum cellularum penetratio.
Sequentia
H Pro Pro-Leu-Ser-Gln-Glu-Ser-Asp-Leu-Trp-Lys-Leu-Lys-Lys-Trp-Lys-Met-Arg-Asn-Gln-Phe-Trp-Val-Lys-Val-Gln-Arg-Gly-OH
CAS Number
1159861-00-3
Formulae hypotheticae
C188H293N53O44S
M. Pondus
4031.7990
Inquisitionis PNC-27
1.Mechanismus Actionis et Membranae Disruptionis
Hanc obligationem solvens permittit ad plenam restitutionem dapibus actionis p53; regulatio comprehensiva variarum actionum cancer cellularum in gradu genetico sequitur, suppressio omnium morborum progressionis finis effectus.
The release of p53 then inhibits cancer cell generation, direct apoptosis being one of the end effects.
Subsequent studies focused on the internal mechanism of PNC-27 inhibiting cancer cells within cells.
Research revealed direct disruption of the cancer cell’s plasma membrane – rapid, near irreversible death is induced, with very minimal to no residual effects on normal cells.
Binding to HDM-2 leads PNC-27 (saltem ex parte) to change conformation.
Oligomerization and pore formation is believed to be the final step in this process.
2.Specific Binding
The very specific and high-affinity recognition of HDM-2 by PNC-27 is what makes this peptide so effective.
Release of p53 activity is the primary and central goal of the entire mechanism.
3.Selectively Kills Cancer Cells
PNC specifically binds to abnormally expressed HDM-2 on cancer cells, excitato osmotic inaequalitate et subsequente membrana dissolutione.
Hoc ultimo ducit ad tumorem cellulam; directus cancer cellae immedicabile mors efficitur, celeri mechanism.
Egregie, membranae cellulae normales tantum vestigium exprimunt quantitates huius HDM-2, ut sanus cellulis non affectus.
Disruptio corporis membranae ipsae cellulae est quae efficit hanc homicidium directum – meatus p53-mediatos intracellulares significationis apoptoseos innixi sunt ab hoc processu omnino separati.
Neglegens status cellulae cancri p53 gene (ferox-genus, mutatur, aut aliter inactivated), dum detectable HDM-II expressio in membrana, PNC-XXVII efficaciter tribue.
Efficiens targeting of cancer cellulis possibilis est, etiam elaborata resistentia tam conventionali chemotherapy quam variis formis radiotherapiae; Praesent p53 maior causa est talis resistentiae.
Novum therapeuticum consilium de tumoribus tractandis repugnantibus sic aperitur hac singulari mechanismo actionis..
COA
HPLC
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