Cloning of a bcl-2 homologue by interaction with adenovirus E1B 19K

Farrow, Stuart N.; White, J. L.; Martinou, Isabelle; Raven, Thomas; Pun, K. Tao; Grinham, C J; Martinou, Jean‐Claude; Brown, R. Dale

doi:10.1038/374731a0

Cited by 475 publications

(264 citation statements)

References 26 publications

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“…Sajjadi et al (19) have shown that the activation of A 3 receptors with the agonist IB-MECA in U-937 cells inhibits the release of TNF-α, which in turn may induce apoptosis. Apoptosis is accompanied by the appearance of bak protein (18). Bak, a member of the bcl-2 family, was found to accelerate cell death in neurons deprived of nerve growth factor and may also be related to the effects of TNF-α (18).…”

Section: Resultsmentioning

confidence: 99%

Adenosine A3Receptor Agonists Protect HL-60 and U-937 Cells from Apoptosis Induced by A3Antagonists

Yao

Sei

Abbracchio

et al. 1997

Biochemical and Biophysical Research Communications

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Section: Resultsmentioning

confidence: 99%

Adenosine A3Receptor Agonists Protect HL-60 and U-937 Cells from Apoptosis Induced by A3Antagonists

Yao

Sei

Abbracchio

et al. 1997

Biochemical and Biophysical Research Communications

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“…There is precedent for this type of dual role with other members of the Bcl2 family. For example, the recently identi®ed family member Bak can promote cell death in some cell types, while promoting cell viability in others (Chittenden et al, 1995;Farrow et al, 1995;Kiefer et al, 1995). Furthermore, Bax has been speculated to have a role in promoting cell death when present as a homodimer, while having a role in maintaining cell viability when present as a heterodimer with Bcl2 (Yang and Korsmeyer, 1996).…”

Section: Discussionmentioning

confidence: 99%

Induction of BCL2 family member MCL1 as an early response to DNA damage

et al. 1997

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When ML-1 human myeloid leukemia cells are exposed to DNA damaging agents, they exhibit dramatic changes in the expression of a variety of gene products. This includes an increase in p53 (wild-type), a decrease in BCL2, a p53-dependent increase in the BCL2 family member BAX, and increases in Growth Arrest and DNA Damage-inducible (GADD) genes such as GADD45; these changes occur as early events in a sequence that culminates in DNA damage-induced apoptosis. DNA damaging agents have now been tested for e ects on expression of another BCL2 family member, MCL1, a gene expressed during ML-1 cell di erentiation. Expression of MCL1 was found to increase upon exposure of ML-1 cells to various types of DNA damaging agents, including ionizing radiation, ultraviolet radiation, and alkylating drugs. The increase in MCL1 occurred rapidly and was transient, levels of the MCL1 mRNA being elevated within 4 h and having returned to near baseline within 24 h. An increase in the Mcl1 protein was also seen, with the maximal increase occurring at an intermediate dose of IR (5 Gray) and lesser increases occurring at either lower or higher doses. The increase in expression of MCL1 was further studied using a panel of human cell lines that includes cells containing or not containing alterations in p53 as well as cells sensitive or insensitive to the apoptosis-inducing e ects of DNA damage. The DNA damage-induced increase in MCL1 mRNA did not depend upon p53 as it was seen in cells lacking functional p53. However, the increase did depend upon susceptibility to apoptosis as it was not seen in cells insensitive to apoptosis-induction by DNA damaging agents. These ®ndings demonstrate that cytotoxic DNA damage causes an increase in the expression of MCL1 along with increases in GADD45 and BAX and a decrease in BCL2. Furthermore, while the increase in GADD45 is seen both in cells that undergo growth arrest and in cells that undergo apoptosis in response to DNA damage, alterations in the pro®le of expression of BCL2 family members occur exclusively in cells that undergo the apoptotic response, with some family members increasing through p53-dependent (BAX) and others through p53-independent (MCL1) pathways. Overall, expression MCL1 can increase during the induction of cell death as well as during the induction of di erentiation.

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“…This is of special interest because viral or bacterial infection in SLE patients is frequently followed by increased disease activity. In addition, we measured expression of bcl-2, FasiAPO-1, and other apoptosis-related gene products, i.e., bcl-x, (43), b m (44), mud (45,46), m m (47)(48)(49), and c-myc (46,(49)(50)(51) or the recently cloned buk (52)(53)(54) and Fas-L (22). In order to investigate whether accelerated in vitro apoptosis is specific to SLE, we tested PBMC from patients with other autoimmune diseases, such as mixed connective tissue disease (MCTD), Wegener's granulomatosis, Takayasu arteritis, and polyarteritis nodosa, with regard to in vitro apoptosis or expression of apoptosis-related gene products.…”

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confidence: 99%

In vitro apoptosis and expression of apoptosis‐related molecules in lymphocytes from patients with systemic lupus erythematosus and other autoimmune diseases

Lorenz

Grünke

Hieronymus

et al. 1997

Arthritis & Rheumatism

169

132

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Objective. To analyze factors related to apoptosis in systemic lupus erythematosus (SLE) peripheral blood mononuclear cells (PBMC) and to compare the findings in SLE PBMC with those in normal donor PBMC or PBMC from patients with other autoimmune diseases. Methods. PBMC from normal healthy donors or patients with SLE, mixed connective tissue disease (MCTD), rheumatoid arthritis (RA), or various vasculitides were isolated. The percentage of apoptosis after activation through different signaling pathways was quantified using propidium iodide staining. Protein expression of Fas/APO‐1 or bcl‐2, and messenger RNA (mRNA) expression of bcl‐2, bcl‐xL, bax, bak, Fas/APO‐1, Fas ligand (Fas‐L), c‐myc, mad, or max were determined. Results. We confirmed previous findings of increased numbers of apoptotic cells in SLE PBMC compared with normal donor cells after in vitro incubation. After activation of PBMC with CD28 monoclonal antibody plus phorbol myristate acetate (CD28 MAb/PMA), staphylococcal enterotoxin B (SEB), or phytohemagglutinin (PHA), the percentage of apoptotic cells was unchanged (SEB) or diminished (CD28 MAb/PMA, PHA) in SLE cells, and the difference between normal donor and SLE cells was less pronounced. On the mRNA level, expression of apoptosis‐related gene products did not differ between SLE cells and normal donor cells. Expression of Fas/APO‐1 protein was increased in freshly isolated SLE T lymphocytes compared with normal donor T lymphocytes, whereas bcl‐2 protein was up‐regulated after a 3‐day culture period. Cellular activation further increased bcl‐2 protein levels, eliminating differences between normal donors and SLE patients. In RA cells, the percentage of apoptosis was similar to that in normal donor PBMC, whereas results using cells from patients with other autoimmune diseases (MCTD, Wegener's granulomatosis, Takayasu arteritis, polyarteritis nodosa) were comparable with those found using SLE PBMC. Addition of growth factors such as interleukin‐2 (IL‐2), IL‐4, or IL‐15 to culture medium decreased the percentage of in vitro apoptosis in both normal donor and SLE cells. Conclusion. Based on these data, we conclude that accelerated in vitro apoptosis and increased Fas/APO‐1 and bcl‐2 protein expression in SLE are nonspecific for the disease, and might be explained at least in part by the increased in vivo activation levels of PBMC from patients with SLE, MCTD, or autoimmune vasculitides combined with in vitro incubation under “noninflammatory” conditions and growth factor withdrawal.

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Cloning of a bcl-2 homologue by interaction with adenovirus E1B 19K

Cited by 475 publications

References 26 publications

Adenosine A3Receptor Agonists Protect HL-60 and U-937 Cells from Apoptosis Induced by A3Antagonists

Adenosine A3Receptor Agonists Protect HL-60 and U-937 Cells from Apoptosis Induced by A3Antagonists

Induction of BCL2 family member MCL1 as an early response to DNA damage

In vitro apoptosis and expression of apoptosis‐related molecules in lymphocytes from patients with systemic lupus erythematosus and other autoimmune diseases

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