Protein Bcl Xl
Mostrando 1-12 de 53 artigos, teses e dissertações.
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1. The anesthetic agent sevoflurane attenuates pulmonary acute lung injury by modulating apoptotic pathways
The objective of this study was to evaluate lung protection by the volatile anesthetic sevoflurane (SEVO), which inhibits apoptosis. Male Sprague-Dawley rats (250–280 g; n=18) were randomly divided into three groups. The LPS group received 5 mg/kg endotoxin (lipopolysaccharide), which induced acute lung injury (ALI). The control (CTRL) group received norma
Braz J Med Biol Res. Publicado em: 20/02/2017
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2. Inibição simultânea dos genes antiapoptóticos Bcl-2 e Bcl-XL em células de leucemia linfoide aguda e células de linfoma do manto mediante RNA de interferência / Simultaneous inhibition of antiapoptóticosBcl-2 and Bcl-XL genes acute lymphocytic leukemia and mantle cell lymphoma by RNA interference
As estatísticas relacionadas aos cânceres hematológicos indicam que a incidência e mortalidade dessas doenças têm aumentado ao longo dos anos. Embora a maioria dos casos de linfomas e leucemias não possua etiologia definida, sugere-se que fatores genéticos possam estar envolvidos. Nesse contexto, destaca-se a família de proteínas Bcl-2, divididas e
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 06/11/2012
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3. Imunoproteção de ilhotas pancreáticas microencapsuladas em biomateriais inovadores e seu potencial terapêutico no diabetes mellitus tipo 1 / Immunoprotection of pancreatic islets microencapsulated in inovative biomaterials and its therapeutic potential in type 1 Diabetes Mellitus
Transplantation of microencapsulated islets represents an attractive therapeutical approach to treat type 1 Diabetes Mellitus, accounting for an improved glycemic control and the abolishment of immunosuppressive therapies. However, maintenance of long-term β-cell viability remains a major problem. During islet isolation, the loss of extracellular matrix
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 08/05/2012
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4. Bcl-2 family proteins expression (Bcl-2, Bcl-xl, Bax, Bak, Bad) in gastric cancer tissue prepared in tissue microarray (TMA) / Imuno-expressão das proteínas da família BCL-2 (BCL-2. BCL-XL, BAX, BAK, BAD) em câncer gátrico, preparados em arranjo em matriz (TMA).
Purpose: To study the immunoexpression of Bcl-2 family proteins (Bcl-2, Bcl-xl, Bax, Bak, Bad) and to evaluate the correlation between the immunoexpression of these proteins with the cleaved caspases 3, Ki-67 and p53 immuno-expression. Methods: A TMA paraffin block was constructed with gastric carcinoma tissue (test group) and normal gastric adjoining mucosa
Publicado em: 2009
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5. The effect of tyrosine-kinase inhibitors on the apoptosis machinery in chronic myeloid leukemia / Efeitos dos inibidores de tirosina-quinase sobre a maquinaria apoptótica na leucemia mielóide crônica
Chronic myeloid leukemia (CML) is a myeloproliferative disease resultant of a clonal expansion of pluripotent hematopoietic stem cells. The CML physiopathology is associated with a translocation between chromosomes 9 and 22 long arms, promoting the formation of a bcr-abl neogene, which codifies the Bcr-Abl protein. The Bcr-Abl oncoprotein presents tyrosine-k
Publicado em: 2007
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6. ROLE OF Bcl-2 AND Bcl-XL IN ANGIOGENESIS
(...)Angiogenesis is defined as the development of new capillaries from pre-existing blood vessels. The hypothesis that tumor growth is angiogenesis dependent was proposed by Judah Folkman in 1971, and it has been confirmed by many investigators thereafter. We have shown that vascular endothelial growth factor (VEGF) induces Bcl-2 expression in endothelial c
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 2006
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7. Vias de sinalização da prolactina em ilhotas de Langerhans de ratos
During pregnancy, panereatie islets undergo a number of structural and functional changes in response to an increased demand for insulin. These changes are orchestrated by several hormones including GH, plaeental lactogens, and prolactin (pRL). Many ofthe alterations observed during pregnancy ean be reproduced in vitro, especially if one uses neonatal islets
Publicado em: 2003
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8. Apoptosis Triggered by Myc-Induced Suppression of Bcl-XL or Bcl-2 Is Bypassed during Lymphomagenesis
Enforced Bcl-2 expression inhibits Myc-induced apoptosis and cooperates with Myc in transformation. Here we report that the synergy between Bcl-2 and Myc in transforming hematopoietic cells in fact reflects a Myc-induced pathway that selectively suppresses the expression of the Bcl-XL or Bcl-2 antiapoptotic protein. Myc activation suppresses Bcl-XL RNA and p
American Society for Microbiology.
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9. Selective regulation of Bcl-XL by a Jak kinase-dependent pathway is bypassed in murine hematopoietic malignancies
Bcl-2 family proteins are key regulators of apoptosis and function as cell death antagonists (e.g., Bcl-2, Bcl-XL, and Mcl-1) or agonists (e.g., Bax, Bad, and Bak). Here we report that among the Bcl-2 family of proteins tested (Bcl-2, Bcl-XL, Mcl-1, Bax, Bad, and Bak), Bcl-XL was unique in that its protein levels were tightly regulated by hemopoietins in bot
Cold Spring Harbor Laboratory Press.
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10. Up-Regulation of Bcl-xl by Hepatocyte Growth Factor in Human Mesothelioma Cells Involves ETS Transcription Factors
Bcl-xl and the hepatocyte growth factor (HGF) receptor c-Met are both highly expressed in mesotheliomas, where they protect cells from apoptosis and can confer resistance to conventional therapeutic agents. In our current study, we investigate a model for the transcriptional control of Bcl-xl that involves ETS transcription factors and the HGF/Met axis. In a
American Society for Investigative Pathology.
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11. Bcl-XL affects Ca2+ homeostasis by altering expression of inositol 1,4,5-trisphosphate receptors
An oligonucleotide-based microarray analysis of 9,500 genes and expressed sequence tags (ESTs) demonstrated that the type 1 inositol 1,4,5-trisphosphate receptor (IP3R) was significantly down-regulated in Bcl-XL-expressing as compared with control cells. This result was confirmed at the mRNA and protein levels by Northern and Western blot analyses of two ind
The National Academy of Sciences.
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12. Bad is a BH3 domain-containing protein that forms an inactivating dimer with Bcl-XL.
The Bcl-2 related protein Bad is a promoter of apoptosis and has been shown to dimerize with the anti-apoptotic proteins Bcl-2 and Bcl-XL. Overexpression of Bad in murine FL5.12 cells demonstrated that the protein not only could abrogate the protective capacity of coexpressed Bcl-XL but could accelerate the apoptotic response to a death signal when it was ex