Evidence map›Paper›PMID 15786732›Full record

ArticleMolecular and cellular biochemistry2005

ARP2 a novel protein involved in apoptosis of LNCaP cells shares a high degree homology with splicing factor Prp8.

J V Tapia-Vieyra, R O Arellano, J Mas-Oliva

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.1field-weighted citation impact, top 51% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Proapoptotic role of novel gene-expression factors.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2007
    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

3 authors at 1 institution in 1 country.

J V Tapia-VieyraInstituto de Fisiología Celular, Universidad Nacional Autónoma de México, México, DF, México.
R O Arellano
J Mas-Oliva
Universidad Nacional Autónoma de México · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mechanism of apoptosis has been recognized as an important event in processes such as cellular development and homeostasis, as well as degenerative conditions like cancer. Prostate cancer during its advanced stages develops androgen independent cells that ultimately overgrow and promote metastatic events. Our group employing androgen independent LNCaP cells have previously proposed, based on electrophysiological findings, that apoptosis induced cells overexpress a cell death calcium channel-like molecule. Here we report the cloning and expression in Xenopus laevis oocytes of apoptosis regulated protein 2 (ARP2), a protein overexpressed in apoptosis induced LNCaP cells capable to induce calcium inward currents and apoptosis typical morphology changes in oocytes injected with arp2 mRNA. Our results also indicate that clone arp2 cDNA (1.3Kb) shares a 99% homology with a small fragment that corresponds to 18% of the complete sequence of Prp8 cDNA (7.0 Kb), a molecule that codifies for an important protein in the assembly of the spliceosome. We propose that protein ARP2 as a fragment of protein Prp8, corresponds to a molecule with a new function in apoptosis related phenomena.

Indexed as

ApoptosisAmino Acid SequenceAnimalsCarrier ProteinsCaspase 3Caspase 7CaspasesCloning, MolecularGene ExpressionHumansMaleMolecular Sequence DataNeoplasm ProteinsOocytesProstatic NeoplasmsRNA-Binding ProteinsCarrier ProteinsCASP3 protein, humanCASP7 protein, humanCaspase 3Caspase 7CaspasesNeoplasm ProteinsPRPF8 protein, humanRNA-Binding Proteins

Identifiers

PMID15786732
OpenAlexW2000977548

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.