Evidence map›Paper›PMID 29995892›Full record

ArticlePLoS genetics2018

Role of Bicaudal C1 in renal gluconeogenesis and its novel interaction with the CTLH complex.

Lucia Carolina Leal-Esteban, Benjamin Rothé, Simon Fortier, Manuela Isenschmid, Daniel B Constam

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. A scATAC-seq atlas of stasis zone in rat skin burn injury wound process.Frontiers in cell and developmental biology · 2024
    Article
  10. Article
  11. Article
  12. Structural and Functional Insights into GID/CTLH E3 Ligase Complexes.International journal of molecular sciences · 2022
    Review
  13. Article
  14. Review
  15. Bicaudal-C Post-transcriptional regulator of cell fates and functions.Frontiers in cell and developmental biology · 2022
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Recognition of nonproline N-terminal residues by the Pro/N-degron pathway.Proceedings of the National Academy of Sciences of the United States of America · 2020
    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

5 authors at 1 institution in 1 country.

Lucia Carolina Leal-EstebanEcole Polytechnique Fédérale de Lausanne (EPFL), School of Life Sciences, Swiss Institute for Experimental Cancer Research (ISREC), Lausanne, Switzerland.ORCID 0000-0002-3618-8346
Benjamin RothéEcole Polytechnique Fédérale de Lausanne (EPFL), School of Life Sciences, Swiss Institute for Experimental Cancer Research (ISREC), Lausanne, Switzerland.ORCID 0000-0002-3191-445X
Simon FortierEcole Polytechnique Fédérale de Lausanne (EPFL), School of Life Sciences, Swiss Institute for Experimental Cancer Research (ISREC), Lausanne, Switzerland.
Manuela IsenschmidEcole Polytechnique Fédérale de Lausanne (EPFL), School of Life Sciences, Swiss Institute for Experimental Cancer Research (ISREC), Lausanne, Switzerland.
Daniel B ConstamEcole Polytechnique Fédérale de Lausanne (EPFL), School of Life Sciences, Swiss Institute for Experimental Cancer Research (ISREC), Lausanne, Switzerland.
École Polytechnique Fédérale de Lausanne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Altered glucose and lipid metabolism fuel cystic growth in polycystic kidneys, but the cause of these perturbations is unclear. Renal cysts also associate with mutations in Bicaudal C1 (Bicc1) or in its self-polymerizing sterile alpha motif (SAM). Here, we found that Bicc1 maintains normoglycemia and the expression of the gluconeogenic enzymes FBP1 and PEPCK in kidneys. A proteomic screen revealed that Bicc1 interacts with the C-Terminal to Lis-Homology domain (CTLH) complex. Since the orthologous Gid complex in S. cerevisae targets FBP1 and PEPCK for degradation, we mapped the topology among CTLH subunits and found that SAM-mediated binding controls Bicc1 protein levels, whereas Bicc1 inhibited the accumulation of several CTLH subunits. Under the conditions analyzed, Bicc1 increased FBP1 protein levels independently of the CTLH complex. Besides linking Bicc1 to cell metabolism, our findings reveal new layers of complexity in the regulation of renal gluconeogenesis compared to lower eukaryotes.

Indexed as

AnimalsAnimals, NewbornBlood GlucoseFructose-BisphosphataseGluconeogenesisGlucoseHEK293 CellsHumansKidneyMiceMice, Inbred C57BLMice, TransgenicMutationPhosphoenolpyruvate Carboxykinase (GTP)Polycystic Kidney DiseasesProtein BindingBicc1 protein, mouseBlood GlucoseFructose-BisphosphataseGlucosePhosphoenolpyruvate Carboxykinase (GTP)RNA-Binding ProteinsRNA, Messenger

Identifiers

PMID29995892
PMCPMC6056059
OpenAlexW2867451337

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.