Evidence map›Paper›PMID 19641504›Full record

ReviewOncogene2008

BIK, the founding member of the BH3-only family proteins: mechanisms of cell death and role in cancer and pathogenic processes.

G Chinnadurai, S Vijayalingam, R Rashmi

Open access · bronzeAbstract readReview
In one paragraph

Review in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

75 citing papers in PubMed, 115 citations in OpenAlex.

  1. Article
  2. A workflow for quantifying cell quiescence in 3D spheroids.Biochemistry and biophysics reports · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. A new era in cancer therapy: targeting the Proteasome-Bcl-2 axis.Journal of experimental & clinical cancer research : CR · 2025
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. PEtOx-DOPE nanoliposomes functionalized with peptide 563 in targetedTurkish journal of biology = Turk biyoloji dergisi · 2024
    Article
  16. Article
  17. Article
  18. Deregulation of apoptotic proteins by induction ofIranian journal of basic medical sciences · 2023
    Article
  19. Article
  20. Article

15 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

G ChinnaduraiInstitute for Molecular Virology, Saint Louis University Health Sciences Center, Doisy Research Center, 1100 South Grand Blvd, St Louis, MO 63104, USA. chinnag@slu.edu
S Vijayalingam
R Rashmi
Saint Louis University · US

Funding

PROMOTION OF CELL SURVIVAL BY ADENOVIRUS E1B 19K PROTEINR01CA033616 · NCI · SAINT LOUIS UNIVERSITY · PI CHINNADURAI, GOVINDASWAMY · 1985 to 2015
$4.0M
ONCOGENIC AND CHEMORESISTANCE BY BCL 2R01CA073803 · NCI · SAINT LOUIS UNIVERSITY · PI CHINNADURAI, GOVINDASWAMY · 1998 to 2008
$2.0M
NCI NIH HHS CA-33616NCI NIH HHS CA-73803NCI NIH HHS R01 CA033616NCI NIH HHS R01 CA073803
6 · The paper itself

Abstract

BIK is the founding member of the BH3-only family pro-apoptotic proteins. BIK is predominantly localized in the ER and induces apoptosis through the mitochondrial pathway by mobilizing calcium from the ER to the mitochondria and remodeling the mitochondrial cristae. BIK-mediated apoptosis is mediated by selective activation of BAX. BIK also induces non-apoptotic cell death in certain cell types by unknown mechanisms. BIK is non-essential for animal development, but appears to be functionally redundant for certain developmental functions with BIM. BIK is implicated in the selection of mature B cells in humans. BIK is a pro-apoptotic tumor suppressor in several human tissues and its expression in cancers is prevented by chromosomal deletions encompassing the Bik locus or by epigenetic silencing. BIK appears to be a critical effector in apoptosis induced by toxins, cytokines and virus infection. Several anti-cancer drugs transcriptionally activate Bik gene expression through transcriptional pathways dependent on factors such as E2F and p53 or by removal of epigenetic marks on the chromatin. BIK appears to be a prominent target for anti-cancer drugs that inhibit proteasomal functions. BIK has also been used as a therapeutic molecule in gene therapy-based approaches to treat difficult cancers.

Indexed as

Adaptor Proteins, Signal TransducingAmino Acid SequenceAnimalsAntineoplastic AgentsApoptosisApoptosis Regulatory Proteinsbcl-2-Associated X ProteinGene Expression RegulationGenetic TherapyHumansMammalsMembrane ProteinsMiceMice, KnockoutMitochondriaMitochondrial ProteinsAdaptor Proteins, Signal TransducingAntineoplastic AgentsApoptosis Regulatory ProteinsBAX protein, humanbcl-2-Associated X ProteinBIK protein, humanBik protein, mouseMembrane ProteinsMitochondrial ProteinsNeoplasm ProteinsTumor Suppressor Proteins

Identifiers

PMID19641504
PMCPMC2928562
OpenAlexW2061727962

What OpenQuestion holds

Textmetadata
LicenceTDM
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.