Results 251 to 260 of about 377,868 (302)
Activator of apoptosis harakiri (HRK) localisation at mitochondria alters mitochondrial morphology independently of other BCL-2 proteins. [PDF]
King LE, Faber L, García-Sáez AJ.
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Current Opinion in Oncology, 2009
Members of the Bcl-2 family of proteins are critical components in regulating the intrinsic apoptotic pathway. Bcl-2 protein overexpression is associated with drug resistance and poor clinical outcome in cancer patients. Preclinical and clinical evaluations demonstrate that downregulation of Bcl-2 restores the intrinsic apoptotic pathways with ...
Mehul P, Patel +3 more
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Members of the Bcl-2 family of proteins are critical components in regulating the intrinsic apoptotic pathway. Bcl-2 protein overexpression is associated with drug resistance and poor clinical outcome in cancer patients. Preclinical and clinical evaluations demonstrate that downregulation of Bcl-2 restores the intrinsic apoptotic pathways with ...
Mehul P, Patel +3 more
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Bcl-2 and Bcl-2-Related Proteins in Apoptosis Regulation
1995In this review we have discussed the importance of Bcl-2 and related proteins in the regulation of apoptotic cell death in mammalian systems. It is clear that Bcl-2 plays a critical role in controlling many forms of PCD. Bcl-2 seems to have particular significance in lymphocyte development and the function of the immune system.
L H, Boise +3 more
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New insights in the role of Bcl-2 Bcl-2 and the endoplasmic reticulum
Apoptosis, 2002The oncogenic protein Bcl-2 which is expressed in membranes of different subcellular organelles protects cells from apoptosis induced by endogenic stimuli. Most of the results published so far emphasise the importance of Bcl-2 at the mitochondria. Several recent observations suggest a role of Bcl-2 at the endoplasmic reticulum (ER).
J, Rudner, V, Jendrossek, C, Belka
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Current Medicinal Chemistry, 2012
Chronic lymphocytic leukemia (CLL) is a common adult leukemia in the Western world with an incidence of 4.2/100,000/year. The clinical course of disease is highly heterogenous; it affects people over 65-70 years of age. This hematologic cancer is characterized by the resistance to apoptosis stimuli predominantly associated with overexpression of ...
M, Rogalinska, Z M, Kilianska
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Chronic lymphocytic leukemia (CLL) is a common adult leukemia in the Western world with an incidence of 4.2/100,000/year. The clinical course of disease is highly heterogenous; it affects people over 65-70 years of age. This hematologic cancer is characterized by the resistance to apoptosis stimuli predominantly associated with overexpression of ...
M, Rogalinska, Z M, Kilianska
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bcl-2 Expression in Pilomatricoma
The American Journal of Dermatopathology, 1997Pilomatricoma is a distinctive tumor characterized by a dual population of proliferating basophilic cells and diagnostic shadow cells, believed to arise from the hair matrix. The normal hair matrix undergoes defined cycles of growth (anagen), regression (catagen), and resting (telogen) that are regulated by programmed cell death (apoptosis). bcl-2 is a
S, Farrier, M, Morgan
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2008
The Bcl2 family of proteins belong to a peculiar class of proteins regulating apoptosis, cell cycle, differentiation, and autophagy; in oncology, the genes coding for these proteins could not be defined neither as dominant transforming oncogenes (such as myc), nor tumor suppressor genes (such as p53).
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The Bcl2 family of proteins belong to a peculiar class of proteins regulating apoptosis, cell cycle, differentiation, and autophagy; in oncology, the genes coding for these proteins could not be defined neither as dominant transforming oncogenes (such as myc), nor tumor suppressor genes (such as p53).
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Bcl-2 Family Immunohistochemistry
2003In recent years, immunohistochemistry as applied to the Bcl-2 family of proteins has represented a burgeoning area of interest to cancer researchers. The majority of studies have focused on the original member Bcl-2, first identified via its involvement in the common t(14;18) chromosomal translocation in B-cell lymphomas (1).
L R, Kelland, P J, Beale
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