Prdm12 Directs Nociceptive Sensory Neuron Development by Regulating the Expression of the NGF Receptor TrkA

Mohamed A. ElTanbouly
Harvard Medical School
January 1, 2019
Cell Rep
https://pubmed.ncbi.nlm.nih.gov/30917309

This article is currently being updated. View its version on PubMed.

https://pubmed.ncbi.nlm.nih.gov/30917309

Research summary

This study demonstrates that Prdm12 is essential for the development of nociceptive sensory neurons by regulating the expression of the nerve growth factor receptor TrkA. Using a Prdm12 conditional Knockout mouse model, the authors show that loss of Prdm12 leads to a significant reduction in TrkA expression, resulting in impaired nociceptor development and function. The findings highlight the critical role of Prdm12 in pain perception pathways.

Key outcome of the study

Prdm12 is crucial for initiating and maintaining TrkA expression in developing nociceptors; its absence leads to defective pain-sensing neuron development.

Mouse model

Prdm12 conditional Knockout mouse model generated by genOway, with targeted deletion of Prdm12 in sensory neurons to study its role in nociceptor development.

TARGET:
PRDM12
PR domain containing 12

Keywords

Nociceptor development, Pain perception, NGF signaling, TrkA expression

Technical specifications

Conditional Knockout, Sensory neuron-specific deletion, Prdm12 gene targeting

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KO repository

>2000 conditional Knockout mouse models for target discovery and  confirmation, in vivo compound specificity, MOA, and clinical studies

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