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Transforming Carcinogenesis is Essential Substrate Accumulation/Interactivity Dimension in Ubiquitin-Proteasomal Dysfunction

Volume 6 - Issue 3

lawrence M Agius*

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    • Department of Pathology, University of Malta Medical School, Europe

    *Corresponding author: lawrence M Agius, Department of Pathology, University of Malta Medical School , Europe

Received: June 07, 2018;   Published: July 05, 2018

DOI: 10.26717/BJSTR.2018.06.001357

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Abstract

The constitutive susceptibilities to malignant transformation are well illustrated by the evolving dimensions of a dysfunctional ubiquitin proteasomal participation in generative reformulation of carcinogenetic pathways of interactivity. Further considerations indicate the transformation as derivative dysfunctional ubiquitin proteasomal system for further transformation. The multilayered complexities of such changes attest for redistribution of protein intermediates within various cellular subcompartments as signified by endosomal and nuclear systems of cooperative interchange. Dynamics formulation is itself a parametric measurement in substitution modelling of substrates as indeed projected within system profile for further change.Theincremental disjunction of such formulasareproposed alternative systems in further parahomeostatic dysregulation in carcinogenesis as a primary generative induction as signified by further developmental adaptation of such systems as DNA repair pathways.

Keywords: Carcinogenetic; Parahomeostatic; Proteasomal System; Leukemogenesis; Myeloid; Homeostasis; Endosomes; Ubiquitin; Tumor; Phosphorylation

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