Evidence map›Paper›PMID 22865860›Full record

ArticleThe Journal of biological chemistry2012

Identification and characterization of an extramitochondrial human 3-hydroxy-3-methylglutaryl-CoA lyase.

Christa Montgomery, Zhengtong Pei, Paul A Watkins, Henry M Miziorko

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Identification of IPF specific genes expressed by lung tissue-derived fibroblasts using next generation sequencing.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2026
    Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
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

4 authors at 3 institutions in 1 country.

Christa MontgomeryDivision of Molecular Biology and Biochemistry, University of Missouri, Kansas City, Missouri 64110, USA.
Zhengtong Pei
Paul A Watkins
Henry M Miziorko
Johns Hopkins University · USKennedy Krieger Institute · USUniversity of Missouri–Kansas City · US

Funding

HMG-COA CYCLE CONTROL IN NORMAL AND DIABETIC LIVERR01DK021491 · NIDDK · UNIVERSITY OF MISSOURI KANSAS CITY · PI MIZIORKO, HENRY M · 1986 to 2004
$1.6M
HMG-COA CYCLE CONTROL IN NORMAL AND DIABETIC LIVERR37DK021491 · NIDDK · MEDICAL COLLEGE OF WISCONSIN · PI MIZIORKO, HENRY M · 1991 to 1999
–
NICHD NIH HHS HD020461NIDDK NIH HHS DK21491NIDDK NIH HHS R01 DK021491NIDDK NIH HHS R37 DK021491
6 · The paper itself

Abstract

3-Hydroxy-3-methylglutaryl-CoA lyase-like protein (HMGCLL1) has been annotated in the Mammalian Genome Collection as a previously unidentified human HMG-CoA lyase (HMGCL). To test the validity of this annotation and evaluate the physiological role of the protein, plasmids were constructed for protein expression in Escherichia coli and Pichia pastoris. Protein expression in E. coli produced insoluble material. In contrast, active HMGCLL1 could be recovered upon expression in P. pastoris. Antibodies were prepared against a unique peptide sequence found in the N terminus of the protein. In immunodetection experiments, the antibodies discriminated between HMGCLL1 and mitochondrial HMGCL. Purified enzyme was characterized and demonstrated to cleave HMG-CoA to acetoacetate and acetyl-CoA with catalytic and affinity properties comparable with human mitochondrial HMGCL. The deduced HMGCLL1 sequence contains an N-terminal myristoylation motif; the putative modification site was eliminated by construction of a G2A HMGCLL1. Modification of both proteins was attempted using human N-myristoyltransferase and [(3)H]myristoyl-CoA. Wild-type protein was clearly modified, whereas G2A protein was not labeled. Myristoylation of HMGCLL1 affects its cellular localization. Upon transfection of appropriate expression plasmids into COS1 cells, immunofluorescence detection indicates that G2A HMGCLL1 exhibits a diffuse pattern, suggesting a cytosolic location. In contrast, wild-type HMGCLL1 exhibits a punctate as well as a perinuclear immunostaining pattern, indicating myristoylation dependent association with nonmitochondrial membrane compartments. In control experiments with the HMGCL expression plasmid, protein is localized in the mitochondria, as anticipated. The available results for COS1 cell expression, as well as endogenous expression in U87 cells, indicate that HMGCLL1 is an extramitochondrial hydroxymethylglutaryl-CoA lyase.

Indexed as

Acyl Coenzyme AAnimalsCatalysisCell Line, TumorChlorocebus aethiopsCOS CellsEnergy MetabolismEscherichia coliFemaleHumansKetone BodiesKetonesLipidsLipogenesisMaleMitochondria3-hydroxy-3-methylglutaryl-coenzyme A3-hydroxy-3-methylglutaryl-coenzyme A lyaseAcyl Coenzyme AHMGCLL1 protein, humanKetone BodiesKetonesLipidsOxo-Acid-LyasesPeptides

Identifiers

PMID22865860
PMCPMC3460428
OpenAlexW2036530052

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.