Evidence map›Paper›PMID 33789102›Full record

ArticleCell reports2021

Loss of Prdm12 during development, but not in mature nociceptors, causes defects in pain sensation.

Mark A Landy, Megan Goyal, Katherine M Casey, Chen Liu, Helen C Lai

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. A compendium of validated pain genes.WIREs mechanisms of disease · 2022
    Review
  14. Review
  15. Genetic pain loss disorders.Nature reviews. Disease primers · 2022
    Review
  16. PRDM12 in Health and Diseases.International journal of molecular sciences · 2021
    Review
  17. 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.

Mark A LandyDepartment of Neuroscience, UT Southwestern Medical Center, Dallas, TX 75390, USA.
Megan GoyalDepartment of Neuroscience, UT Southwestern Medical Center, Dallas, TX 75390, USA.
Katherine M CaseyDepartment of Neuroscience, UT Southwestern Medical Center, Dallas, TX 75390, USA.
Chen LiuDepartment of Neuroscience, UT Southwestern Medical Center, Dallas, TX 75390, USA; Department of Internal Medicine, Hypothalamic Research Center, Dallas, TX 75390, USA.
Helen C LaiDepartment of Neuroscience, UT Southwestern Medical Center, Dallas, TX 75390, USA. Electronic address: helen.lai@utsouthwestern.edu.
Southwestern Medical Center · US

Funding

Hypothalamic Serotonin Receptors and Olanzapine-induced Metabolic SyndromeR01DK114036 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI Chen Liu · 2017 to 2026
$4.2M
Elucidating the logic of proprioceptive networksR01NS100741 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI LAI, HELEN · 2018 to 2022
$1.8M
Elucidating the role of Prdm12 in the development and maintenance of nociceptive neuronsF31NS111796 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI LANDY, MARK · 2019 to 2020
$65k
NIDDK NIH HHS R01 DK114036NINDS NIH HHS F31 NS111796NINDS NIH HHS R01 NS100741
6 · The paper itself

Abstract

Prdm12 is a key transcription factor in nociceptor neurogenesis. Mutations of Prdm12 cause congenital insensitivity to pain (CIP) from failure of nociceptor development. However, precisely how deletion of Prdm12 during development or adulthood affects nociception is unknown. Here, we employ tissue- and temporal-specific knockout mouse models to test the function of Prdm12 during development and in adulthood. We find that constitutive loss of Prdm12 causes deficiencies in proliferation during sensory neurogenesis. We also demonstrate that conditional knockout from dorsal root ganglia (DRGs) during embryogenesis causes defects in nociception. In contrast, we find that, in adult DRGs, Prdm12 is dispensable for most pain-sensation and injury-induced hypersensitivity. Using transcriptomic analysis, we find mostly unique changes in adult Prdm12 knockout DRGs compared with embryonic knockout and that PRDM12 is likely a transcriptional activator in the adult. Overall, we find that the function of PRDM12 changes over developmental time.

Indexed as

Embryonic DevelopmentPain PerceptionAgingAnimalsCarrier ProteinsCell ProliferationEmbryo, MammalianExonsGanglia, SpinalGene Expression Regulation, DevelopmentalHumansMiceMice, Inbred C57BLMice, KnockoutNerve Tissue ProteinsNociceptionCarrier ProteinsNerve Tissue ProteinsPrdm12 protein, mouseRepressor Proteinsbehaviorcongenital insensitivity to painDRGmousenociceptorspainpainlessnessPrdm12sensory neurogenesis

Identifiers

PMID33789102
PMCPMC8048104
OpenAlexW3146166722

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.