What are the exceptions of trp channels?
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Transient Receptor Potential (TRP) channels, a diverse superfamily of non-selective cation channels, have exceptions in their composition. One notable exception is the TRPN channels, which are exclusively found in invertebrates and fish, not in mammalian genomes . Another exception lies in the fact that most mammalian TRP channels, with the exception of two members, are Ca2+-permeable non-selective cation channels that can be constitutively active or gated by various physicochemical stimuli . These exceptions highlight the diversity within the TRP channel superfamily, showcasing unique characteristics and functions that contribute to their involvement in a wide array of physiological processes and cellular functions.
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25 Citations | TRP channels exceptions are two mammalian members that are not Ca2+-permeable cation channels. They are involved in diverse physiological functions and are potential drug therapy targets. |
TRP channels are exceptions in non-excitable cells, responsible for various physiological functions like phagocytosis and microglia activation, modulating neuropathic pain, body temperature, and cancer cell migration. | |
The exceptions of TRP channels are TRPN channels, exclusively found in invertebrates and fish, while all six subfamilies (TRPV, TRPC, TRPM, TRPA, TRPML, TRPP) are present in mammalian genomes. | |
Not addressed in the paper. |
Related Questions
Zinc and TRPC6 channels relationship?8 answersThe relationship between zinc and Transient Receptor Potential Canonical 6 (TRPC6) channels is multifaceted, involving zinc's role in modulating TRPC6 channel function and the channel's capacity to regulate zinc homeostasis within cells. TRPC6 channels, known for their involvement in various physiological and pathological processes, have been shown to facilitate zinc influx, which in turn influences cellular functions and disease outcomes.
TRPC6-specific zinc influx has been demonstrated to potentiate β-adrenoceptor-stimulated positive inotropy in rodent cardiomyocytes, highlighting a crucial role in cardiac function and suggesting a therapeutic potential for chronic heart failure. Similarly, in the context of renal ischemia/reperfusion (I/R) injury, TRPC6-mediated zinc influx has been shown to attenuate cell death and inflammation by modulating pyroptosis-related proteins and inflammasome activity, thereby protecting against renal damage. This protective mechanism is further supported by findings that TRPC6 overexpression in HEK-293 cells leads to intracellular zinc accumulation, affecting cellular zinc buffering capacities and influencing the expression of proteins related to zinc homeostasis.
Moreover, TRPC6 channels have been implicated in the transport of zinc in the placenta, affecting fetal development and pregnancy outcomes. TRPC6 deficiency in mice resulted in altered placental structure and function, as well as perturbations in zinc and iron homeostasis in various organs. In the nervous system, nano-ZnO has been shown to activate TRPC6 channels, increasing calcium influx and autophagy in neuroblastoma cells, suggesting a potential anticancer mechanism but also raising concerns about nanomaterial biosecurity. Additionally, TRPC6 activation by hyperforin, a component of St. John's Wort, has been shown to mobilize zinc from internal pools, further illustrating the complex interplay between TRPC6 channels and zinc in neuronal function and antidepressant action.
In summary, the relationship between zinc and TRPC6 channels encompasses regulatory mechanisms that affect cellular and systemic physiological processes, with implications for understanding and treating various diseases.
How is the TRPV1 Channel linked to Alzheimer's Disease progression?5 answersThe TRPV1 channel plays a crucial role in Alzheimer's Disease (AD) progression through various mechanisms. TRPV1 deficiency in AD models leads to neuroprotective effects by activating the BDNF/CREB pathway, preventing hippocampal apoptosis. Additionally, TRPV1 activation rescues Aβ-tolerant microglial dysfunction, restores immune responses, and reduces amyloid pathology and memory deficits in AD mice models. TRPV1 activation induces autophagy, regulates metabolism, and decreases amyloid and tau pathology, reversing memory deficits in AD mice. Moreover, TRPV1 modulation of lipid metabolism alleviates ApoE4-induced immune dysfunction, rescues memory impairment, and improves neuronal autophagy in AD models. Furthermore, PcActx peptide, a TRPV1 modulator, inhibits amyloid-related proteins, prevents calcium response, and activates the Akt/Gsk3β-mediated Nrf2 pathway, showing promise as a therapeutic agent for AD.
What are invertebrates organisms in which the TRP channels have been explored?5 answersTRP channels in invertebrate organisms have been explored in the following phyla: mollusks, parasitic helminths, choanoflagellates, sponges, Cnidaria, Lophotrochozoa, and arthropods, and schistosomes.
Is beta tubulin 3 involved in TRP channel interaction?5 answersBeta tubulin 3 (β-tubulin 3) is involved in the interaction with TRP channels. The study by Rostovtseva et al. demonstrated that β-tubulin constructs, particularly β3, effectively block the voltage-dependent anion channel (VDAC) of the mitochondrial outer membrane, which is a TRP channel. Additionally, the study by Huai et al. showed that TRPV4, a TRP channel, associates with tubulin beta 5 in transfected cells. These findings suggest that β-tubulin isoforms, including β3 and beta 5, play a role in the interaction with TRP channels.
Does TRPV2 interact with microtubules?5 answersTRPV2 interacts with microtubules. The interaction between TRPV2 and microtubules is important for neurite initiation, extension, and branching events. TRPV2 localizes in specific subcellular regions enriched with filamentous actin, such as growth cones, filopodia, lamellipodia, and neurites. TRPV2 regulates actin cytoskeleton and interacts with soluble actin. The interaction between TRPV2 and microtubules is evolutionary and has functional significance. TRPV2 also interacts with tubulin beta 5, which may play a role in mechanosensation and neuropathic pain. The interaction between TRPV2 and microtubules is mediated through two novel tubulin-binding motifs in the TRPV2 C-terminus.
What are the mechanisms by which TRP channels mediate chemosensation?5 answersTRP channels mediate chemosensation through various mechanisms. They are involved in the detection of chemical stimuli in the oronasal cavities, which contribute to the perception of flavor and trigeminality. TRP channels are activated by chemical compounds, resulting in sensations related to texture, temperature, and pungency. Additionally, TRP channels play a role in nociception and pain, responding to thermal and electrophile stimuli. Some TRP channels are also involved in mechanosensation, responding to changes in membrane stretch and osmotically induced cell swelling or shrinkage. The activation of TRP channels is complex and can be polymodal, with different channels responding to unique forms of activation energy. Overall, TRP channels are crucial in mediating chemosensation by detecting and transducing chemical stimuli into sensory signals.