Evidence map›Paper›PMID 21189256›Full record

ArticleThe Journal of biological chemistry2011

Amphipathic tail-anchoring peptide and Bcl-2 homology domain-3 (BH3) peptides from Bcl-2 family proteins induce apoptosis through different mechanisms.

Jae-Kyun Ko, Kyoung-Han Choi, Jun Peng, Feng He, Zhi Zhang, Noah Weisleder, Jialing Lin, Jianjie Ma

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

15 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Curcumin and Gastric Cancer: a Review on Mechanisms of Action.Journal of gastrointestinal cancer · 2019
    Review
  3. Wild-type p53-modulated autophagy and autophagic fibroblast apoptosis inhibit hypertrophic scar formation.Laboratory investigation; a journal of technical methods and pathology · 2018
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Resveratrol induces apoptosis in K562 cells via the regulation of mitochondrial signaling pathways.International journal of clinical and experimental medicine · 2015
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
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

8 authors at 2 institutions in 1 country.

Jae-Kyun KoDepartment of Physiology and Biophysics, Robert Wood Johnson Medical School, Piscataway, New Jersey 08854, USA.
Kyoung-Han Choi
Jun Peng
Feng He
Zhi Zhang
Noah Weisleder
Jialing Lin
Jianjie Ma
University of Oklahoma Health Sciences Center · USJohnson University · US

Funding

Ca Sparks in Muscle Aging and DystrophyR01AG028614 · NIA · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI MA, JIANJIE · 2006 to 2016
$4.1M
Structure-Function of Bcl-2 Related Apoptosis Regulators in MembranesR01GM062964 · NIGMS · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI LIN, JIALING · 2001 to 2014
$3.3M
Store-Operated Calcium Entry and ApoptosisR01CA095739 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI MA, JIANJIE · 2001 to 2010
$2.3M
Calcium Regulation in the Progression of Muscular DystrophyR00AR054793 · NIAMS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI WEISLEDER, NOAH · 2011 to 2013
$730k
Calcium Regulation in the Progression of Muscular DystrophyK99AR054793 · NIAMS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI WEISLEDER, NOAH · 2008 to 2009
$159k
NCI NIH HHS R01 CA095739NCI NIH HHS R01-CA095739NIAMS NIH HHS K99 AR054793NIAMS NIH HHS K99/R00-AR054793NIAMS NIH HHS R00 AR054793NIA NIH HHS R01 AG028614NIA NIH HHS R01-AG028614NIGMS NIH HHS GM062964NIGMS NIH HHS R01 GM062964
6 · The paper itself

Abstract

Bcl-2 homology domain-3 (BH3) peptides are potent cancer therapeutic reagents that target regulators of apoptotic cell death in cancer cells. However, their cytotoxic effects are affected by different expression levels of Bcl-2 family proteins. We recently found that the amphipathic tail-anchoring peptide (ATAP) from Bfl-1, a bifunctional Bcl-2 family member, produced strong pro-apoptotic activity by permeabilizing the mitochondrial outer membrane. Here, we test whether the activity of ATAP requires other cellular factors and whether ATAP has an advantage over the BH3 peptides in targeting cancer cells. Confocal microscopic imaging illustrates specific targeting of ATAP to mitochondria, whereas BH3 peptides show diffuse patterns of cytosolic distribution. Although the pro-apoptotic activities of BH3 peptides are largely inhibited by either overexpression of anti-apoptotic Bcl-2 or Bcl-xL or nullification of pro-apoptotic Bax and Bak in cells, the pro-apoptotic function of ATAP is not affected by these cellular factors. Reconstitution of synthetic ATAP into liposomal membranes results in release of fluorescent molecules of the size of cytochrome c from the liposomes, suggesting that the membrane permeabilizing activity of ATAP does not require additional protein factors. Because ATAP can target to the mitochondrial membrane and its pro-apoptotic activity does not depend on the content of Bcl-2 family proteins, it represents a promising candidate for anti-cancer drugs that can potentially overcome the intrinsic apoptosis-resistant nature of cancer cells.

Indexed as

Antineoplastic AgentsApoptosisbcl-X ProteinCytochromes cHeLa CellsHumansLiposomesMinor Histocompatibility AntigensMitochondrial MembranesNeoplasmsPeptide FragmentsPermeabilityProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2Antineoplastic AgentsBax protein (53-86)BCL2L1 protein, humanBCL2-related protein A1bcl-X ProteinCytochromes cLiposomesMinor Histocompatibility AntigensPeptide FragmentsProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2

Identifiers

PMID21189256
PMCPMC3059050
OpenAlexW1968755198

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.