Evidence map›Paper›PMID 21253851›Full record

ArticleMolecular and cellular biochemistry2011

Deletion mutational analysis of BMRP, a pro-apoptotic protein that binds to Bcl-2.

Srinivas Malladi, Kishore V L Parsa, Deepthi Bhupathi, María A Rodríguez-González, Juan A Conde, Pallavi Anumula, Hannah E Romo, Cheryl J Claunch, Rafael P Ballestero, Maribel González-García

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Article in Molecular and cellular biochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.1field-weighted citation impact, top 47% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
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  5. Review
  6. Mitochondrial ribosomes in cancer.Seminars in cancer biology · 2017
    Review
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

10 authors at 1 institution in 1 country.

Srinivas MalladiDepartment of Chemistry, Texas A&M University-Kingsville, 700 University Blvd., Kingsville, TX 78363-8202, USA.
Kishore V L Parsa
Deepthi Bhupathi
María A Rodríguez-González
Juan A Conde
Pallavi Anumula
Hannah E Romo
Cheryl J Claunch
Rafael P Ballestero
Maribel González-García
Texas A&M University – Kingsville · US

Funding

Analysis of Proteins that Modulate ApoptosisSC3GM083732 · NIGMS · TEXAS A&M UNIVERSITY-KINGSVILLE · PI GONZALEZ-GARCIA, MARIBEL · 2008 to 2011
$404k
NIGMS NIH HHS 1SC3GM083732NIGMS NIH HHS S06 GM08127-28
6 · The paper itself

Abstract

Bcl-2 is an anti-apoptotic member of the Bcl-2 family of proteins that protects cells from apoptosis induced by a large variety of stimuli. The protein BMRP (MRPL41) was identified as a Bcl-2 binding partner and shown to have pro-apoptotic activity. We have performed deletion mutational analyses to identify the domain(s) of Bcl-2 and BMRP that are involved in the Bcl-2/BMRP interaction, and the region(s) of BMRP that mediate its pro-apoptotic activity. The results of these studies indicate that both the BH4 domain of Bcl-2 and its central region encompassing its BH1, BH2, and BH3 domains are required for its interaction with BMRP. The loop region and the transmembrane domain of Bcl-2 were found to be dispensable for this interaction. The Bcl-2 deletion mutants that do not interact with BMRP were previously shown to be functionally inactive. Deletion analyses of the BMRP protein delimited the region of BMRP needed for its interaction with Bcl-2 to the amino-terminal two-thirds of the protein (amino acid residues 1-92). Further deletions at either end of the BMRP(1-92) truncated protein resulted in lack of binding to Bcl-2. Functional studies performed with BMRP deletion mutants suggest that the cell death-inducing domains of the protein reside mainly within its amino-terminal two-thirds. The region of BMRP required for the interaction with Bcl-2 is very relevant for the cell death-inducing activity of the protein, suggesting that one possible mechanism by which BMRP induces cell death is by binding to and blocking the anti-apoptotic activity of Bcl-2.

Indexed as

ApoptosisMutationSequence DeletionAnimalsBase SequenceBlotting, WesternDNA PrimersHumansMiceMitochondrial ProteinsNIH 3T3 CellsProtein BindingProto-Oncogene Proteins c-bcl-2Ribosomal ProteinsTwo-Hybrid System TechniquesDNA PrimersMitochondrial ProteinsMRPL41 protein, humanProto-Oncogene Proteins c-bcl-2Ribosomal Proteins

Identifiers

PMID21253851
OpenAlexW2062408850

What OpenQuestion holds

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Registered trials

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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.