Evidence map›Paper›PMID 19559032›Full record

ArticleJournal of molecular biology2009

High-yield heterologous expression of wild type and mutant Ca(2+) ATPase: Characterization of Ca(2+) binding sites by charge transfer.

Yueyong Liu, Rajendra Pilankatta, David Lewis, Giuseppe Inesi, Francesco Tadini-Buoninsegni, Gianluca Bartolommei, Maria Rosa Moncelli

Open access · greenAbstract read
In one paragraph

Article in Journal of molecular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

16 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Phosphatidylserine flipping by the P4-ATPase ATP8A2 is electrogenic.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  5. Mechanism of the E2 to E1 transition in CaProceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  6. Article
  7. Drug Interactions With the CaFrontiers in molecular biosciences · 2018
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
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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

7 authors at 2 institutions in 2 countries.

Yueyong LiuCalifornia Pacific Medical Center Research Institute, San Francisco, 94107, USA.
Rajendra Pilankatta
David Lewis
Giuseppe Inesi
Francesco Tadini-Buoninsegni
Gianluca Bartolommei
Maria Rosa Moncelli
California Pacific Medical Center · USUniversity of Florence · IT

Funding

Molecular and Cellular Studies of Ca2+ Transport ATPaseR01HL069830 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI INESI, GIUSEPPE · 2002 to 2010
$4.6M
NHLBI NIH HHS R01 HL069830PHS HHS R0 301-69830
6 · The paper itself

Abstract

High-yield heterologous SERCA1 (Ca(2+) ATPase) expression was obtained in COS-1 cells infected with recombinant adenovirus vector (rAdSERCA). Higher transcription and expression were obtained in the presence of a His(6) tag at the amino terminus, as compared with a His(6) tag at the carboxyl SERCA terminus, or no tag. The expressed protein was targeted extensively to intracellular membranes. Optimal yield of functional Ca(2+) ATPase corresponded to 10% of total protein, with phosphoenzyme levels, catalytic turnover and Ca(2+) transport identical with those of native SERCA1. This recombinant membrane-bound (detergent-free) enzyme was used for characterization of Ca(2+) binding at the two specific transmembrane sites (ATP-free) by measurements of net charge transfer upon Ca(2+) binding to the protein, yielding cooperative isotherms (K(1)=5.9+/-0.5x10(5) M(-1) and K(2)=5.7+/-0.3x10(6) M(-1)). Non-cooperative binding of only one Ca(2+), and loss of ATPase activation, were observed following E309 mutation at site II. On the other hand, as a consequence of the site II mutation, the affinity of site I for Ca(2+) was increased (K=4.4+/-0.2x10(6) M(-1)). This change was due to a pK(a) shift of site I acidic residues, and to contributions of oxygen functions from empty site II to Ca(2+) binding at site I. No charge movement was observed following E771Q mutation at site I, indicating no Ca(2+) binding to either site. Therefore, calcium occupancy of site I is required to trigger cooperative binding to site II and catalytic activation. In the presence of millimolar Mg(2+), the charge movement upon addition of Ca(2+) to WT ATPase was reduced by 50%, while it was reduced by 90% when Ca(2+) was added to the E309Q/A mutants, demonstrating that competitive Mg(2+) binding can occur at site I but not at site II.

Indexed as

AdenoviridaeAnimalsBinding SitesCalciumChlorocebus aethiopsCOS CellsGenetic VectorsHumansHydrogen-Ion ConcentrationMagnesiumModels, MolecularMutagenesis, Site-DirectedSarcoplasmic Reticulum Calcium-Transporting ATPasesTranscription, GeneticCalciumMagnesiumSarcoplasmic Reticulum Calcium-Transporting ATPases

Identifiers

PMID19559032
PMCPMC2928698
OpenAlexW1967279158

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.