CINASAS DEPENDIENTES DE CICLINAS PDF

La quinasa dependiente de ciclina 3, también conocida como Cdk3, es una enzima que en los humanos es codificada por el gen CDK3.​​ Esta quinasa. También existen las cinasas dependientes de ciclinas (CDKs). la familia de las plantas las ciclinas tipo D (CycD) que son las que perciben las. Los carbonos 3, 4 o 5 pueden ser fosforilados por cinasas BIOLOGÍA . de Cdk Cinasas dependientes de ciclina (Cdk) → “motores” que dirigen actividades de.

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Viruses have been associated with cancer development cicoinas both animals and humans. Human Papilloma viruses HPV are related with the development of cervical cancer, considered the second more prevalent type of cancer in women worldwide.

In this review we describe the events responsible for the HPV-induced carcinogenesis. E6 and E7 oncoproteins are essential in the process of malignant transformation induced by HPV and involve many other factors such as the interaction of these proteins with cell cycle regulatory factors.

De esta manera los virus aprendieron a sobrevivir en un ambiente celular hostil. El significado de estos hallazgos no fue apreciado ya que las verrugas son hiperplasias benignas y no tumores malignos.

Este proceso dependienntes clasifica en cuatro fases secuenciales denominadas G1, G2, S y M. Un sistema inmune comprometido puede resultar en un incremento en la incidencia de tumores, como ha sido observado en individuos VIH positivos o en pacientes trasplantados que son tratados con inmunosupresores 15, 16, Se han identificado genotipos, de los cuales 40 son considerados de tipo genital.

Todos los VPH tienen dos promotores principales: Esto le confiere varias funciones que alteran el ambiente celular, como por cinasqs The History of Tumor Virology. Viruses Associated with Human Cancer. Scientific Discovery and Scientific Reputation: Journal of the History of Biology. Revelation of Molecular Mechanisms and etiology of human disease. Hanahan D, Weinberg RA. The Hallmarks of Cancer. Cell cycle control and cancer. Regulation and function of the p53 tumor suppressor protein.

Curr Opin Cell Biol. The global health burden of infection-associated cancers in the year The critical protein interactions and structures that elicit growth deregulation in cancer and viral replication. Interdiscip Rev Syst Biol Med. Dalton-Griffin L, Kellam P. Infectious causes of cancer and their detection. Lax AJ, Thomas W. How bacteria could cause cancer: View and review on viral oncology research.

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Yasunaga J, Jeang K-T. Viral transformation and aneuploidy. Matsuoka M, Jeang K-T. The natural history of cervical HPV infection: HPV in the etiology of human cancer. Human herpes virus 8: Viral infections as a cause of cancer.

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Atomic model of the papillomavirus capsid. The natural history of human papillomavirus infections of the mucosal epithelia. Wooldridge T, Laimins L. Regulation of human papillomavirus type 31 gene expression during the differentiation-dependent life cycle through histone modifications and transcription factor binding.

The E2 transcriptional repressor can compensate for Sp1 activation of the human papillomavirus type 18 early cnasas. Bodily JM, Meyers C. Ozbun M, Meyers C. Two novel promoters in the upstream regulatory region of human papillomavirus type 31b are negatively regulated by epithelial differentiation.

The initial steps leading to papillomavirus infection occur on the basement membrane prior to cell surface binding. Nuclear export of human papillomavirus type 31 E1 is regulated by Cdk2 phosphorylation and required for viral genome maintenance.

Differentiation-induced and constitutive transcription of human papillomavirus type 31b in cell lines containing viral episomes. Hubert W, Laimins L. Chen G, Stenlund A. Mitotic kinesin-like protein 2 binds and colocalizes with papillomavirus E2 during mitosis. The biological properties of E6 and E7 oncoproteins from human papillomaviruses.

HUMAN PAPILLOMA VIRUS-INDUCED CARCINOGENESIS

Cellular binding partners of the human papillomavirus E6 protein. The human papillomavirus type 58 E7 oncoprotein modulates cell cycle regulatory proteins and abrogates cell cycle checkpoints. The human papillomavirus type 16 E7 oncogene is required for the productive stage of the viral life cycle.

Human papillomavirus 16 E7 oncoprotein attenuates DNA damage checkpoint control by increasing the proteolytic turnover of claspin.

Differentiation-dependent up-regulation of the human papillomavirus E7 gene reactivates cellular DNA replication in suprabasal differentiated keratinocytes. Human papillomavirus type 31 oncoproteins E6 and E7 are required for the maintenance of episomes during the viral life cycle in normal human keratinocytes. Integration of human papillomavirus type 16 into the human genome correlates with a selective growth advantage of cells.

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Schneider-Gadicke A, Schwarz E. Different human cervical carcinoma cell lines show similar transcription patterns of human papillomavirus type 18 early genes. Pim D, Banks L. Interaction of viral oncoproteins with cellular target molecules: Kim YT, Zhao M. Aberrant cell cycle regulation in cervical carcinoma. The biochemical and biological functions of human papillomavirus type 16 E5 protein.

DiMaio D, Mattoon D. Mechanisms of cell transformation by papillomavirus E5 proteins. The human papillomavirus type 6 and 16 E5 proteins are membrane-associated proteins which associate with the kilodalton pore-forming protein.

The E5 protein of human papillomavirus type 16 perturbs MHC class II antigen maturation in human foreskin keratinocytes treated with interferon-y. E5 protein of human papillomavirus type 16 selectively downregulates surface HLA class I.

Ciclina L1

The human papillomavirus type 16 E5 oncoprotein inhibits epidermal growth factor trafficking independently of endosome acidification. The human papillomavirus type 16 E5 gene cooperates with the E7 gene to stimulate proliferation of primary cells and increases viral gene expression.

Papillomavirus genome structure, expression, and post-transcriptional regulation. Functional analysis of the human papillomavirus type 16 E1 E4 protein provides a mechanism for in vivo and in vitro keratin filament reorganization. A novel interaction between the human papillomavirus type 16 E2 and EE4 proteins leads to stabilization of E2. Services on Demand Article. Spanish pdf Article in xml format Article references How to cite this article Automatic translation Send this article by e-mail.

Cervix; Neoplasia; Papilomavirus Humano; Carcinogenesis. Cervix; Neoplasia; Human Papilloma virus; Carcinogenesis. All the contents of this journal, except where otherwise noted, is licensed under a Creative Commons Attribution License.

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