Evidence map›Paper›PMID 11417471›Full record

ReviewLeukemia2001

Unwinding the loop of Bcl-2 phosphorylation.

M V Blagosklonny

Abstract readComparative StudyReview
PubMed Publisher
In one paragraph

Review in Leukemia, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.7field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

48 citing papers in PubMed, 125 citations in OpenAlex.

  1. Article
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  6. Inhibition of induced-hepatic cancerFrontiers in oncology · 2022
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  10. MDA-9/Syntenin regulates protective autophagy in anoikis-resistant glioma stem cells.Proceedings of the National Academy of Sciences of the United States of America · 2018
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

M V BlagosklonnyMedicine Branch, Building 10, R 12N226, National Cancer Institute, NIH, Bethesda, MD 20892, USA.
National Cancer Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent evidence indicates that anti-apoptotic functions of BcI-2 can be regulated by its phosphorylation. According to the 'mitotic arrest-induced' model, multi-site phosphorylation of the BcI-2 loop domain is followed by cell death. In contrast, in cytokine-dependent cell lines, cytokines mediate phosphorylation of BcI-2 on S70, preventing apoptosis. As discussed in this review, these models are not mutually exclusive but reflect different cellular contexts. During mitotic arrest, signal transduction is unique and is fundamentally different from classical mitogenic signaling, since the nucleus membrane is dissolved, gene expression is reduced, and numerous kinases and regulatory proteins are hyperphosphorylated. Hyperphosphorylation of BcI-2 mediated by paclitaxel and other microtubule-active drugs is strictly dependent on targeting microtubules that in turn cause mitotic arrest. In addition to serine-70 (S70), microtubule-active agents promote phosphorylation of S87 and threonine-69 (T69), inactivating BcI-2. A major obstacle for identification of the mitotic BcI-2 kinase(s) is that inhibition of putative kinase(s) by any means (dominant-negative mutants, antisense oligonucleotides, pharmacological agents) may arrest cycle, preventing mitosis and BcI-2 phosphorylation. The role of BcI-2 phosphorylation in cell death is discussed.

Indexed as

Protein Processing, Post-TranslationalApoptosisbcl-X ProteinEnzyme ActivationHumansInterleukin-3MicrotubulesMitosisModels, BiologicalMyeloid Cell Leukemia Sequence 1 ProteinNeoplasm ProteinsPaclitaxelPhosphorylationProtein KinasesProtein Structure, TertiaryProto-Oncogene Proteins c-bcl-2BCL2L1 protein, humanbcl-X ProteinInterleukin-3Myeloid Cell Leukemia Sequence 1 ProteinNeoplasm ProteinsPaclitaxelProtein KinasesProto-Oncogene Proteins c-bcl-2

Identifiers

PMID11417471
OpenAlexW2331801728

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.