Evidence map›Paper›PMID 30830403›Full record

ArticleMetabolomics : Official journal of the Metabolomic Society2018

Mitochondrial aconitase is a key regulator of energy production for growth and protein expression in Chinese hamster ovary cells.

Neha Dhami, Drupad K Trivedi, Royston Goodacre, David Mainwaring, David P Humphreys

Abstract read
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In one paragraph

Article in Metabolomics : Official journal of the Metabolomic Society, 2018. 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
–field-weighted citation impact
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.

  1. Cuproptosis in iron overload hepatocytes.Cell death & disease · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Advances of Glycometabolism Engineering in Chinese Hamster Ovary Cells.Frontiers in bioengineering and biotechnology · 2021
    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

5 authors.

Neha DhamiProtein Sciences, UCB, 216 Bath Road, Slough, Berkshire, SL1 3WE, UK. neha.dhami@ucb.com.
Drupad K TrivediManchester Institute of Biotechnology and School of Chemistry, University of Manchester, 131 Princess Street, Manchester, M1 7DN, UK.
Royston GoodacreManchester Institute of Biotechnology and School of Chemistry, University of Manchester, 131 Princess Street, Manchester, M1 7DN, UK.
David MainwaringProtein Sciences, UCB, 216 Bath Road, Slough, Berkshire, SL1 3WE, UK.
David P HumphreysProtein Sciences, UCB, 216 Bath Road, Slough, Berkshire, SL1 3WE, UK.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionMammalian cells like Chinese hamster ovary (CHO) cells are routinely used for production of recombinant therapeutic proteins. Cells require a continuous supply of energy and nutrients to sustain high cell densities whilst expressing high titres of recombinant proteins. Cultured mammalian cells are primarily dependent on glucose and glutamine metabolism for energy production.

objectivesThe TCA cycle is the main source of energy production and its continuous flow is essential for cell survival. Modulated regulation of TCA cycle can affect ATP production and influence CHO cell productivity.

methodsTo determine the key metabolic reactions of the cycle associated with cell growth in CHO cells, we transiently silenced each gene of the TCA cycle using RNAi.

resultsSilencing of at least four TCA cycle genes was detrimental to CHO cell growth. With an exception of mitochondrial aconitase (or Aco2), all other genes were associated with ATP production reactions of the TCA cycle and their resulting substrates can be supplied by other anaplerotic and cataplerotic reactions. This study is the first of its kind to have established key role of aconitase gene in CHO cells. We further investigated the temporal effects of aconitase silencing on energy production, CHO cell metabolism, oxidative stress and recombinant protein production.

conclusionTransient silencing of mitochondrial aconitase inhibited cell growth, reduced ATP production, increased production of reactive oxygen species and reduced cell specific productivity of a recombinant CHO cell line by at least twofold.

Indexed as

Aconitate HydrataseAdenosine TriphosphateAnimalsCell ProliferationCHO CellsCricetulusMitochondriaAconitate HydrataseAdenosine TriphosphateCHO cellsGlucose metabolismm-AconitaseOxidative stressTCA cycle

Identifiers

What OpenQuestion holds

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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.