Inscrição na biblioteca: Guest
Portal Digital Begell Biblioteca digital da Begell eBooks Diários Referências e Anais Coleções de pesquisa
Critical Reviews™ in Eukaryotic Gene Expression
Fator do impacto: 2.156 FI de cinco anos: 2.255 SJR: 0.649 SNIP: 0.599 CiteScore™: 3

ISSN Imprimir: 1045-4403
ISSN On-line: 2162-6502

Volumes:
Volume 30, 2020 Volume 29, 2019 Volume 28, 2018 Volume 27, 2017 Volume 26, 2016 Volume 25, 2015 Volume 24, 2014 Volume 23, 2013 Volume 22, 2012 Volume 21, 2011 Volume 20, 2010 Volume 19, 2009 Volume 18, 2008 Volume 17, 2007 Volume 16, 2006 Volume 15, 2005 Volume 14, 2004 Volume 13, 2003 Volume 12, 2002 Volume 11, 2001 Volume 10, 2000 Volume 9, 1999 Volume 8, 1998 Volume 7, 1997 Volume 6, 1996 Volume 5, 1995 Volume 4, 1994

Critical Reviews™ in Eukaryotic Gene Expression

DOI: 10.1615/CritRevEukarGeneExpr.v22.i4.70
pages 345-358

Lysosomes, Growth Factor Activity, and Carcinogenic Implications

Marvin Melzer
self-employed

RESUMO

The aim of this paper is to point out a body of literature which up to now has been largely ignored by investigators in the area of growth factors This paper will offer a response to the questions: Why is it that inhibition of endolysosomal proteases (by agents such as leupeptin, methylamine, etc.) or inhibition of endocytosis block the activities of all growth factors and carcinogens so far studied? What role therefore can endocytosis and endolysosomes (E/L) play in the signal transduction process? As will be detailed below, in many cases involving growth factors, inhibition of E/L proteases results in complete or very significant loss of growth factor activity. That is, treatment with inhibitors of E/L proteases (i.e., leupeptin, antipain methylamine, etc.) erases the normal activity of growth factors affecting systems of concern to immunologists, endocrinologists, and cardiologists. There are strong indications in the literature that suggest that in the nervous system (of obvious interest to neuroscientists) endocytosis plays a vital role in the induced proliferation of neurons as well (of interest to neurologists). This paper will explore the implications and offer an explanation for these findings. Thus this communication will travel from one growth factor to another in order to demonstrate the universality of the model offered in this paper.


Articles with similar content:

Molecular Epidemiology of Human Cancer: Biomarkers of Genotoxic Exposure and Susceptibility
Journal of Environmental Pathology, Toxicology and Oncology, Vol.20, 2001, issue 4
Stephen G. Grant
Hard Science Versus Phenomenology in Reproductive Immunology
Critical Reviews™ in Immunology, Vol.19, 1999, issue 5-6
David A. Clark
Complex Interplay Between Aging and Cancer: Role of TGF-β Signaling
Critical Reviews™ in Oncogenesis, Vol.22, 2017, issue 3-4
Panagiotis Papageorgis
Cancer and Cancer Stem Cells: New Molecular Perspectives
Critical Reviews™ in Oncogenesis, Vol.24, 2019, issue 1
Onur Sahin, Gokce Ceren Kuscu, Gulperi Oktem, Elif Tunc, Funda Cagirir Dindaroglu, Cevik Gurel, Ismet Hortu, Gizem Inetas, Aylin Buhur
Mechanism and Consequences of δ-Opioid Receptor Internalization
Critical Reviews™ in Neurobiology, Vol.17, 2005, issue 1
Rudiger Schulz, Daniela A. Eisinger