Evidence map›Paper›PMID 24894176›Full record

ReviewCurrent molecular medicine2014

The characteristics of Bax inhibitor-1 and its related diseases.

B Li, R K Yadav, G S Jeong, H-R Kim, H-J Chae

Open access · bronzeAbstract readReview
In one paragraph

Review in Current molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Characterization of theInternational journal of molecular sciences · 2024
    Article
  4. Review
  5. [Bax inhibitor-1 inhibits calcification of vascular smooth muscle cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021
    Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. PeerJ · 2017
    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

5 authors at 3 institutions in 3 countries.

B Li
R K Yadav
G S Jeong
H-R Kim
H-J Chae(H.-R. Kim) Department of Dental Pharmacology, School of Dentistry, Wonkwang University, Iksan, 570-749, Republic of Korea. hrkimdp@wonkwang.ac.kr.
Jeonbuk National University · KRBinzhou Medical University · CNWonkwang University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bax inhibitor-1 (BI-1) is an evolutionarily-conserved endoplasmic reticulum protein. The expression of BI-1 in mammalian cells suppresses apoptosis induced by Bax, a pro-apoptotic member of the Bcl-2 family. BI-1 has been shown to be associated with calcium (Ca(2+)) levels, reactive oxygen species (ROS) production, cytosolic acidification, and autophagy as well as endoplasmic reticulum stress signaling pathways. According to both in vitro and clinical studies, BI-1 promotes the characteristics of cancers. In other diseases, BI-1 has also been shown to regulate insulin resistance, adipocyte differentiation, hepatic dysfunction and depression. However, the roles of BI-1 in these disease conditions are not fully consistent among studies. Until now, the molecular mechanisms of BI-1 have not directly explained with regard to how these conditions can be regulated. Therefore, this review investigates the physiological role of BI-1 through molecular mechanism studies and its application in various diseases.

Indexed as

AnimalsApoptosis Regulatory ProteinsEndoplasmic Reticulum StressHumansLysosomesMembrane ProteinsModels, BiologicalReactive Oxygen SpeciesUnfolded Protein ResponseApoptosis Regulatory ProteinsMembrane ProteinsReactive Oxygen SpeciesTMBIM6 protein, human

Identifiers

PMID24894176
PMCPMC4083451
OpenAlexW2105395511

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.