Nociceptor-specific gene deletion reveals a major role for Nav1.7 (PN1) in acute and inflammatory pain.

By Mohammed A. Nassar, L. Stirling, G. Forlani, M. Baker, E. Matthews, A. Dickenson, J. Wood. Proceedings of the National Academy of Sciences of the United States of America, 2004

687 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology, Sensory Systems

View Paper: https://www.semanticscholar.org/paper/e0aaff4d5b4d174b4ae8ba3e2ed680bca49c594e

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. D. Julius
2. A. Basbaum
3. D. Bautista
4. Grégory Scherrer
5. R. Medzhitov

In Physiology

1. D. Julius
2. D. Bautista
3. A. Basbaum
4. Grégory Scherrer
5. Arne May
6. R. Medzhitov
7. Clifford J. Woolf

In Sensory Systems

1. D. Julius
2. D. Bautista
3. A. Basbaum
4. Grégory Scherrer
5. Clifford J. Woolf
6. Ardem Patapoutian
7. Arne May
8. R. Medzhitov

Citations in the corpus

• SCN9A mutations in paroxysmal extreme pain disorder: allelic variants underlie distinct channel defects and phenotypes. (2006, neutral): “7 mediates a tetrodotoxin (TTX) -sensitive, fast-inactivating current and has a role in acute and inflammatory pain (Nassar et al., 2004).”
• Cellular and Molecular Mechanisms of Pain (2009, positive): “7 in C nociceptors supports a key role for this channel in mechanical and thermal hypersensitivity after inflammation, and in acute responses to noxious mechanical stimuli (Nassar et al., 2004).”
• Burn injury: Challenges and advances in burn wound healing, infection, pain and scarring (2018, background): “7 knockoutmice – particularly, in states of inflammation induced nociception [159,160].”