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1.
Indian J Exp Biol ; 2005 Dec; 43(12): 1130-8
Artículo en Inglés | IMSEAR | ID: sea-58400

RESUMEN

The migration of B16LuF1 cells, B16-melanoma cells of lower metastatic potential to lung was enhanced through artificial basement membrane in presence of gangliosides of B16LuF1 cells as well as gangliosides of B16-melanoma cells of higher metastatic potential to lung, namely, B16LuF5 and B16LuF10 cells. The same concentration (50 microM) of gangliosides of B16LuF1, B16LuF5 and B16LuF10 cells gradually increased the migration of B16LuF1 cells through basement membrane. Moreover, B16LuF10 cell gangliosides modified the migratory effect of laminin and fibronectin on B16LuF1 cells. Laminin alone increased migration of B16LuF1 cells whereas fibronectin alone decreased migration of the same cells. When B16LuF10 cell gangliosides were used in combination with fibronectin, gangliosides removed the migration inhibitory effect of fibronectin resulting in net enhancing effect. Gangliosides in association with laminin also increased the enhancing effect of laminin on migration of B16LuF1 cells. Thus, gangliosides showed additive enhancing effect when used in combination with laminin. However, effect of individual gangliosides were different. Out of six gangliosides isolated from B16LuF10 cells only two gangliosides corresponding to standard gangliosides GM2 and GM3 enhanced migration of B16LuF1 cells. The migration of B16LuF1 cells in presence of each of the remaining four gangliosides corresponding to GT1b, GD1b, GD1a and GM1 was not altered and was comparable to that of untreated control. Thus, gangliosides of B16 melanoma cells alone or in combination with laminin or fibronectin enhanced migration of B16 melanoma cells through artificial basement membrane, suggesting possible role of tumor gangliosides during invasion of metastatic tumor cells through basement membrane of the surrounding tissues in vivo.


Asunto(s)
Animales , Membrana Basal/patología , Línea Celular Tumoral , Movimiento Celular/fisiología , Cromatografía en Capa Delgada , Densitometría , Fibronectinas/fisiología , Gangliósido G(M2)/fisiología , Gangliósido G(M3)/fisiología , Laminina/fisiología , Neoplasias Pulmonares/patología , Melanoma Experimental/metabolismo , Membranas Artificiales , Ratones
2.
Korean Journal of Pediatrics ; : 1360-1363, 2004.
Artículo en Coreano | WPRIM | ID: wpr-46058

RESUMEN

Tay-Sachs disease is an autosomal recessive, neurodegenerative disorder that results from excessive storage of the cell membrane glycolipid, and GM2 ganglioside within the lysosomes of cells. This disease is caused by deficiency of the isoenzyme beta-hexosaminidase A, produced in the endoplasmic reticulum. Patients with Tay-Sachs disease are characterized by normal motor development in the first few months of life, followed by progressive weakness and loss of motor skills beginning around 2 to 6 months of life. Neurodegeneration is relentless, with death occurring by the age of 4 or 5 years. Tay-Sachs disease could be diagnosed by hexosaminidase enzyme assay and DNA analysis of HEXA gene. However, specific treatment has not been developed. We report here on a case of Tay- Sachs disease in 18-month-old male who presented with delayed development and seizure. This patient showed hyperacusis and cherry red spot in macula on examination of the fundus. The hexosaminidase A activity was zero percent in the enzymatic assay and DNA analysis identified a mutation that glutamine is substituted by stop codon at position 390(Q390X). This patient is the first case of Tay-Sachs disease in Korea diagnosed by enzymatic assay and DNA analysis.


Asunto(s)
Humanos , Lactante , Masculino , beta-N-Acetilhexosaminidasas , Membrana Celular , Codón de Terminación , ADN , Retículo Endoplásmico , Pruebas de Enzimas , Gangliósido G(M2) , Glutamina , Hexosaminidasa A , Hexosaminidasas , Hiperacusia , Corea (Geográfico) , Lisosomas , Destreza Motora , Enfermedades Neurodegenerativas , Prunus , Convulsiones , Enfermedad de Tay-Sachs
3.
J. Liga Bras. Epilepsia ; 8(1): 7-14, 1995. ilus
Artículo en Portugués | LILACS | ID: lil-152207

RESUMEN

Com avanços recentes da genética molecular, um número cada vez maior de genes responsáveis por diversas doenças hereditárias têm sido localizados. O conhecimento gerado por essas pesquisas está saindo dos laboratórios e sendo rapidamente aplicado na prática clínica. Neste artigo alguns conceitos básicos de genética molecular, com ênfase nos estudos de ligaçäo genética, säo revistos. Estes conceitos säo fundamentais para o entendimento das descobertas recentes no campo da genética das epilepsias. A seguir, as síndromes epilépticas cuja localizaçäo cromossômica já foi determinada säo discutidas. Algumas formas de epilepsia que näo foram ainda localizadas, mas que säo foco de intenso estudo, säo também apresentadas. Finalmente, algumas consideraçöes sobre as aplicaçöes práticas dessas novas descobertas säo discutidas brevemente


Asunto(s)
Humanos , Epilepsia/genética , Ligamiento Genético , Biología Molecular , Epilepsias Mioclónicas , Epilepsias Parciales , Gangliósido G(M2) , Hemangioma Cavernoso , Lipofuscinosis Ceroideas Neuronales , Convulsiones , Enfermedad de Tay-Sachs , Esclerosis Tuberosa
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