mProX™ Human MRGPRD Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
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Published Data
Fig.1 The shielding benefits of L-BAIBA against osteocyte vitality are channeled via MRGPRD.
Mrgprd knockdown with siRNA diminishes the safeguarding impact of L-BAIBA on osteocyte viability. ***p < 0.001 compared to vehicle/H2O2, ###p < 0.001 compared to negative control/H2O2, and +++p < 0.001 compared to Mrgprd siRNA/H2O2.
Ref: Kitase, Yukiko, et al. "β-aminoisobutyric acid, l-BAIBA, is a muscle-derived osteocyte survival factor." Cell reports 22.6 (2018): 1531-1544.
Pubmed: 29425508
DOI: 10.1016/j.celrep.2018.01.041
Research Highlights
Wang B, et al. "Sensory neuron-specific long noncoding RNA in small non-peptidergic dorsal root ." Life sciences, 2023.
The study aimed to investigate the role of a sensory neuron-specific long noncoding RNA (SS-lncRNA) in repairing nerve injury-induced mechanical hypersensitivity. The experiments involved the downregulation and rescue of SS-lncRNA in small non-peptidergic dorsal root ganglion (DRG) neurons, followed by spinal nerve ligation (SNL) and mechanical stimulation. Findings showed that restoring SS-lncRNA in these neurons reversed the reduction of the calcium-activated potassium channel subfamily N member 1 (KCNN1) induced by SNL and alleviated mechanical hypersensitivity. Conversely, mimicking SS-lncRNA downregulation in these DRG neurons enhanced mechanical response without affecting thermal and cold nociceptive hypersensitivities, likely through silencing KCNN1 expression by altering the interactions between SS-lncRNA and lysine-specific demethylase 6B (KDM6B). These results highlight the importance of SS-lncRNA in nerve injury-induced symptoms and suggest its potential as a therapeutic target for neuropathic pain patients.
Pubmed:
37741322
DOI:
10.1016/j.lfs.2023.122120
Wang L, et al. "Involvement of Mrgprd-expressing nociceptors-recruited spinal mechanisms in nerve ." iScience, 2023.
The study aimed to investigate the role of mechanically responsive non-peptidergic nociceptors in intractable symptoms of neuropathic pain, such as mechanical allodynia and hyperalgesia. Using a mouse model of nerve injury, the researchers found that ablation of Mrgprd(CreERT2)-marked neurons reduced these symptoms. Electrophysiological recordings revealed that nerve injury opened Abeta-fiber and C-fiber inputs to specific laminae in the spinal cord, and these inputs were attenuated in mice with ablated Mrgprd(+) neurons. Furthermore, activating these neurons drove mechanical allodynia and hyperalgesia. The authors also identified a potential mechanism, involving the dampening of potassium currents, that may contribute to the development of nerve injury-induced mechanical pain. The findings shed light on potential therapeutic targets for pain management.
Pubmed:
37250305
DOI:
10.1016/j.isci.2023.106764
