TRPM3 Antibody - C-terminal region (ARP35608_P050)
- Known as:
- TRPM3 Antibody - C-terminal region (ARP35608_P050)
- Catalog number:
- arp35608_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- TRPM3 Antibody - C-terminal region (ARP35608_P050)
Related genes to: TRPM3 Antibody - C-terminal region (ARP35608_P050)
- Gene:
- TRPM3 NIH gene
- Name:
- transient receptor potential cation channel subfamily M member 3
- Previous symbol:
- -
- Synonyms:
- KIAA1616, LTRPC3, GON-2
- Chromosome:
- 9q21.12-q21.13
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-11
- Date modifiied:
- 2018-02-13
Related products to: TRPM3 Antibody - C-terminal region (ARP35608_P050)
Related articles to: TRPM3 Antibody - C-terminal region (ARP35608_P050)
- Transient receptor potential vanilloid 1 (TRPV1) was the first noxious heat-sensitive channel discovered. In rodents, its role is robust in the heat response of the cell body of polymodal nociceptors, but surprisingly small in that of the peripheral terminals in the skin. TRPV1's contribution to the heat threshold depends on anatomical localisation, being prevalent in the tail while absent in the hind paw of the mouse. In behavioural tests of rodents, the role of TRPV1 is marginal with lower, but significant with higher, temperatures. In contrast to the basal heat response, inflammatory heat hyperalgesia/allodynia critically depends on TRPV1. In contrast to rats and mice, TRPV1 receptor antagonists elevate the heat pain threshold in humans, potentially leading to scald injuries and precluding their clinical use. TRPM3 and anoctamin 1 are other heat-sensitive channels that play limited roles in rodents' noxious heat responsiveness. The function of the cold- and heat-activated TRPA1 channel in heat sensation is a matter of debate. In contrast, TRPV2, TRPV3, TRPV4 and TRPM2 channels are unlikely to be major determinants of noxious heat sensation. Combined genetic ablation of TRPV1, TRPA1 and TRPM3 in the mouse results in a near-complete reduction of the heat response; however, the heat threshold remains unchanged. In humans, however, combined pharmacological block of the three TRP channels elevates the noxious heat threshold in skin by only 1°C. TRPV1 appears to be the only known heat sensor with an established but limited role in heat pain sensation; thus, other heat sensor must also contribute. - Source: PubMed
Publication date: 2026/05/26
Pethő GáborReeh Peter W - Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a multisystemic illness, commonly associated with dysregulation of the immune system including reduced cytotoxicity of natural killer (NK) cells and post-exertional neuroimmune exhaustion. Previously, transient receptor potential melastatin 3 (TRPM3) ion channel impairment associated with reduced Ca mobilisation in NK cells from ME/CFS patients was reported. To further explore the pathomechanisms involved in ME/CFS, we investigated the downstream impact of TRPM3 ion channel dysfunction on mitochondrial Ca mobilisation in NK cells. - Source: PubMed
Publication date: 2026/05/23
Magawa Chandi TabethEaton-Fitch NatalieMuraki KatsuhikoMarshall-Gradisnik Sonya - This study investigated the transcriptomic changes in the jejunum and pancreas of broiler chickens fed a diet supplemented with sugarcane bagasse (SB) to elucidate the physiological response of broilers to insoluble dietary fiber. - Source: PubMed
Publication date: 2026/05/22
Asiamah Collins AmponsahKheravii Sarbast KMusigwa SostheneWu Shu-Biaode Las Heras-Saldana Sara - In many tissues, stem cells are found lining fluid-filled cavities, and their neighboring niche cells include cells with beating cilia. However, the role of mechanical forces created by cilia beating on stem cells remains elusive. We developed an approach to transiently inhibit the cilia beating of ependymal cells (ECs) lining the forebrain ventricle by injecting magnetic bead-coupled antibodies targeting EC cilia and then applying a magnetic field. We show that EC cilia beating enforces neural stem cell (NSC) quiescence through mechano-sensitive polycystin 1/2 (PKD1/2)- and transient receptor potential melastatin 3 (TRPM3)-mediated Ca transients. Only a few hours of EC cilia beating inhibition triggered NSC activation in vivo. CRISPR-Cas9-mediated deletion of TRPM3 or PKD1/2 in NSCs phenocopied the effect of EC cilia beating inhibition, whereas pharmacological activation of TRPM3 rescued NSC quiescence in the absence of cilia beating. Our data reveal that mechanical forces generated by EC cilia beating regulate NSC quiescence/activation dynamics. - Source: PubMed
Publication date: 2026/05/13
Bressan CedricGengatharan ArchanaRodriguez-Aller RaquelRichter Maria LSnapyan MarinaFischer-Sternjak JudithRoukerd Maryam RezaeezadehRosin NicoleCherinet AbigailBiernaskie JeffHabibi EhsanGötz MagdalenaSaghatelyan Armen - Osteoarthritis (OA) is a degenerative joint disease characterized by chronic pain. We investigated whether the ion channel transient receptor potential melastatin 3 (TRPM3), expressed in sensory neurons, mediates OA pain. - Source: PubMed
Publication date: 2026/05/09
da Costa RobsonPereira SuelenGentry CliveDias Fabiana CAlmeida Bianca de LimaMaurer MargotPrimicheru Laura IMoreira LioMannebach StefanieWeissgerber PetraPhilipp Stephan EAndersson David ABevan Stuart