ArticleGenes & development1998
Selective regulation of Bcl-XL by a Jak kinase-dependent pathway is bypassed in murine hematopoietic malignancies.
Article in Genes & development, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 105 citations in OpenAlex.
- Rhabdomyosarcoma: Current Therapy, Challenges, and Future Approaches to Treatment Strategies.Cancers · 2023Review
- Roles and Regulation of BCL-xL in Hematological Malignancies.International journal of molecular sciences · 2022Review
- Review
- Identification of Candidate Signature Genes and Key Regulators Associated With Trypanotolerance in the Sheko Breed.Frontiers in genetics · 2019Article
- Genetically defining the mechanism of Puma- and Bim-induced apoptosis.Cell death and differentiation · 2012Article
- Brain-derived neurotrophic factor enhances Bcl-xL expression through protein kinase casein kinase 2-activated and nuclear factor kappa B-mediated pathway in rat hippocampus.Brain pathology (Zurich, Switzerland) · 2011Article
- A novel requirement for Janus kinases as mediators of drug resistance induced by fibroblast growth factor-2 in human cancer cells.PloS one · 2011Article
- BH3-only proteins and their effects on cancer.Advances in experimental medicine and biology · 2010Review
- Dexamethasone inhibits camptothecin-induced apoptosis in C6-glioma via activation of Stat5/Bcl-xL pathway.Biochimica et biophysica acta · 2009Article
- Deregulation of c-Myc Confers distinct survival requirements for memory B cells, plasma cells, and their progenitors.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- Article
- Distinct promoters mediate constitutive and inducible Bcl-XL expression in malignant lymphocytes.Oncogene · 2007Article
- Article
- Article
- Roles of Bim in apoptosis of normal and Bcr-Abl-expressing hematopoietic progenitors.Molecular and cellular biology · 2004Article
- Myc pathways provoking cell suicide and cancer.Oncogene · 2003Review
- The Bcl-2 family: roles in cell survival and oncogenesis.Oncogene · 2003Review
- c-Myc augments gamma irradiation-induced apoptosis by suppressing Bcl-XL.Molecular and cellular biology · 2003Article
- Normal and leukemic hematopoiesis: are leukemias a stem cell disorder or a reacquisition of stem cell characteristics?Proceedings of the National Academy of Sciences of the United States of America · 2003Review
- In BCR-ABL-positive cells, STAT-5 tyrosine-phosphorylation integrates signals induced by imatinib mesylate and Ara-C.Leukemia · 2003Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
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 both immortal and primary myeloid progenitors. Investigating signaling pathways utilized by cytokine receptors established that the regulation of Bcl-XL protein levels is mediated by the Jak kinase pathway and is independent of other signaling effectors including STATs, PI-3' kinase, and Ras. Moreover, we provide the first direct evidence that Bcl-X is altered in cancer, because bcl-X expression was activated selectively by retroviral insertions in murine myeloid and T-cell hemopoietic malignancies. Tumors harboring bcl-X insertions had altered bcl-X RNAs, expressed elevated levels of Bcl-XL protein, and lacked the requirements for cytokines normally essential for cell survival. Finally, overexpression of Bcl-XL effectively protected IL-3-dependent myeloid cells from apoptosis following removal of trophic factors. Therefore, Bcl-XL functions as a key cytokine regulated anti-apoptotic protein in myelopoiesis and contributes to leukemia cell survival.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.