イノシトール1,4,5-三リン酸受容体、イノシトール三リン酸受容体、イノシトール三リン酸レセプター、イノシトール3リン酸受容体、イノシトール3リン酸レセプター、IP3 receptor、IP3R
WordNet
- a cellular structure that is postulated to exist in order to mediate between a chemical agent that acts on nervous tissue and the physiological response
- an optically inactive alcohol that is a component of the vitamin B complex
PrepTutorEJDIC
- =sense organ / 受信装置
UpToDate Contents
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- 1. T細胞受容体シグナル伝達 t cell receptor signaling
- 2. 血小板生物学 platelet biology
- 3. インスリン様成長因子 Iの生理学 physiology of insulin like growth factor i
- 4. 肥満細胞：表面受容体とシグナル伝達 mast cells surface receptors and signal transduction
- 5. ペプチドホルモンのシグナル伝達および調節 peptide hormone signal transduction and regulation
English Journal
- RGS2 regulates urotensin II-induced intracellular Ca2+ elevation and contraction in glomerular mesangial cells.
- Adebiyi A.Author information Department of Physiology, University of Tennessee Health Science Center, Memphis, Tennessee.AbstractUrotensin II (UII), a vasoactive peptide modulates renal hemodynamics. However, the physiological functions of UII in glomerular cells are unclear. In particular, whether UII alters mesangial tone remains largely unknown. The present study investigates the physiological effects of UII on glomerular mesangial cells (GMCs). This study also tested the hypothesis that the regulator of G-protein signaling (RGS) controls UII receptor (UTR) activity in GMCs. RT-PCR, Western immunoblotting, and immunofluorescence revealed UTR expression in cultured murine GMCs. Mouse UII (mUII) stimulated Ca(2+) release from intracellular stores and activated store-operated Ca(2+) entry (SOCE) in the cells. mUII also caused a reduction in planar GMC surface area. mUII-induced [Ca(2+)]i elevation and contraction were attenuated by SB 657510, a UTR antagonist, araguspongin B, an inositol 1,4,5-trisphosphate receptor antagonist, thapsigargin, a sarco/endoplasmic reticulum Ca(2+)-ATPase inhibitor, and La(3+), a store-operated Ca(2+) channel blocker, but not nimodipine, an L-type Ca(2+) channel blocker. In situ proximity ligation assay indicated molecular proximity between endogenous RGS2 and UTR in the cells. Treatment of GMCs with mUII elevated plasma membrane expression of RGS2 by ∼2-fold. mUII also increased the interaction between RGS2 and UTR in the cells. siRNA-mediated knockdown of RGS2 in murine GMCs increased mUII-induced [Ca(2+)]i elevation and contraction by ∼35 and 31%, respectively. These findings indicate that mUII-induced SOCE results in murine GMC contraction. These data also suggest that UTR activation stimulates RGS2 recruitment to GMC plasma membrane as a negative feedback mechanism to regulate UTR signaling.
- Journal of cellular physiology.J Cell Physiol.2014 Apr;229(4):502-11. doi: 10.1002/jcp.24470.
- Urotensin II (UII), a vasoactive peptide modulates renal hemodynamics. However, the physiological functions of UII in glomerular cells are unclear. In particular, whether UII alters mesangial tone remains largely unknown. The present study investigates the physiological effects of UII on glomerular
- PMID 24105430
- The role of mechanical tension on lipid raft dependent PDGF-induced TRPC6 activation.
- Lei L1, Lu S1, Wang Y2, Kim T2, Mehta D3, Wang Y4.Author information 1Department of Bioengineering & Beckman Institute for Advanced Science and Technology, University of Illinois, Urbana-Champaign, Urbana, IL 61801, United States; Department of Bioengineering & Institute of Engineering in Medicine, University of California, San Diego, La Jolla, CA 92093, United States.2Department of Bioengineering & Beckman Institute for Advanced Science and Technology, University of Illinois, Urbana-Champaign, Urbana, IL 61801, United States.3Department of Pharmacology, College of Medicine, University of Illinois, Chicago, IL 60612, United States.4Department of Bioengineering & Beckman Institute for Advanced Science and Technology, University of Illinois, Urbana-Champaign, Urbana, IL 61801, United States; Department of Bioengineering & Institute of Engineering in Medicine, University of California, San Diego, La Jolla, CA 92093, United States. Electronic address: yiw015@eng.ucsd.edu.AbstractCanonical transient receptor potential channel 6 (TRPC6) can play an important role in governing how cells perceive the surrounding material environment and regulate Ca(2+) signaling. We have designed a TRPC6 reporter based on fluorescence resonance energy transfer (FRET) to visualize the TRPC6-mediated calcium entry and hence TRPC6 activity in live cells with high spatiotemporal resolutions. In mouse embryonic fibroblasts (MEFs), platelet-derived growth factor BB (PDGF) can activate the TRPC6 reporter, mediated by phospholipase C (PLC). This TRPC6 activation occurred mainly at lipid rafts regions of the plasma membrane because disruption of lipid raft/caveolae by methyl-β-cyclodextrin (MβCD) or the expression of dominant-negative caveolin-1 inhibited the TRPC6 activity. Culturing cells on soft materials or releasing the intracellular tension by ML-7 reduced this PDGF-induced activation of TRPC6 without affecting the PDGF-regulated Src or inositol 1,4,5-trisphosphate (IP3) receptor function, suggesting a specific role of mechanical tension in regulating TRPC6. We further showed that the release of intracellular tension had similar effect on the diffusion coefficients of TRPC6 and a raft marker, confirming a strong coupling between TRPC6 and lipid rafts. Therefore, our results suggest that the TRPC6 activation mainly occurs at lipid rafts, which is regulated by the mechanical cues of surrounding materials.
- Biomaterials.Biomaterials.2014 Mar;35(9):2868-77. doi: 10.1016/j.biomaterials.2013.12.030. Epub 2014 Jan 4.
- Canonical transient receptor potential channel 6 (TRPC6) can play an important role in governing how cells perceive the surrounding material environment and regulate Ca(2+) signaling. We have designed a TRPC6 reporter based on fluorescence resonance energy transfer (FRET) to visualize the TRPC6-medi
- PMID 24397990
- Hypersensitive mAChRs are Involved in the Epiphora of Transplanted Glands.
- Ding C1, Cong X, Zhang Y, Yang NY, Li SL, Wu LL, Yu GY.Author information 1Center Laboratory and Center for Salivary Gland Diseases, Peking University School and Hospital of Stomatology, 22 Zhong Guan Cun South St., Beijing, 100081, P.R. China.AbstractAutologous transplantation of the submandibular gland is an effective treatment for severe dry eye syndrome. However, more than 40% of patients experience epiphora 3 to 6 months after transplantation. The underlying mechanism of epiphora remains to be elucidated. To investigate the potential roles of muscarinic acetylcholine receptors (mAChRs) in the induction of epiphora in transplanted glands, we assessed and found elevated mRNA and protein expression of M1- and M3-mAChR in transplanted glands from epiphora patients. The content of inositol 1, 4, 5-trisphosphate was also elevated. Moreover, carbachol (5 and 10 µM) induced greater increase of [Ca2+]i in isolated epiphora submandibular cells than in controls. Although aquaporin-5 (AQP5) content and distribution in the apical and lateral plasma of epiphora glands did not change, AQP5 content was reduced in lipid microdomains (lipid rafts and caveolae) but increased in non-lipid microdomains compared with controls. Carbachol (10 µM) increased the ratio of non-lipid microdomain to total AQP5 in the cultured control submandibular gland tissue. Taken together, these results indicated that hypersensitive mAChRs might be involved in the epiphora of transplanted submandibular glands by modulating AQP5 trafficking.
- Journal of dental research.J Dent Res.2014 Mar;93(3):306-312. Epub 2014 Jan 3.
- Autologous transplantation of the submandibular gland is an effective treatment for severe dry eye syndrome. However, more than 40% of patients experience epiphora 3 to 6 months after transplantation. The underlying mechanism of epiphora remains to be elucidated. To investigate the potential roles o
- PMID 24389807
Japanese Journal
- Role of Inositol-1,4,5-Trisphosphate Receptor in the Regulation of Calcium Transients in Neonatal Rat Ventricular Myocytes
- Zeng Zheng,Zhang Heping,Lin Na [他]
- Journal of pharmacological sciences 126(1), 37-46, 2014-09
- NAID 40020200052
- Role of Inositol-1,4,5-Trisphosphate Receptor in the Regulation of Calcium Transients in Neonatal Rat Ventricular Myocytes
- Zeng Zheng,Zhang Heping,Lin Na,Kang Man,Zheng Yuanyuan,Li Chen,Xu Pingxiang,Wu Yongquan,Luo Dali
- Journal of Pharmacological Sciences 126(1), 37-46, 2014
- … This study determined the regulatory effect of inositol 1,4,5-trisphosphate receptors (IP3Rs) on the basal Ca2+ transients in cardiomyocytes. …
- NAID 130004677803
- EthanolによるType 1 IP_3 Receptors (IP_3Rs-1)の発現調節機構
- 水野 晃治,黒川 和宏,大熊 誠太郎
- 日本神経精神薬理学雑誌 = Japanese journal of psychopharmacology 33(4), 161-165, 2013-08-25
- NAID 10031195273
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- This gene encodes an intracellular receptor for inositol 1,4,5-trisphosphate. Upon stimulation by inositol 1,4,5-trisphosphate, this receptor mediates calcium release from the endoplasmic reticulum. Mutations in this gene cause ...
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| リンク元 | 「イノシトール3リン酸受容体」「イノシトール3リン酸レセプター」「イノシトール1,4,5-三リン酸受容体」「イノシトール三リン酸レセプター」「イノシトール1,4,5-トリスリン酸受容体」 |
| 関連記事 | 「trisphosphate」「inositol」 |
「イノシトール3リン酸受容体」
- 英
- inositol 1,4,5-trisphosphate receptor
- 関
- イノシトール三リン酸受容体、イノシトール1,4,5-三リン酸受容体、イノシトール3リン酸レセプター、イノシトール三リン酸レセプター
「イノシトール3リン酸レセプター」
- 英
- inositol 1,4,5-trisphosphate receptor
- 関
- イノシトール三リン酸受容体、イノシトール1,4,5-三リン酸受容体、イノシトール3リン酸受容体、イノシトール三リン酸レセプター
「イノシトール1,4,5-三リン酸受容体」
- 英
- inositol 1,4,5-trisphosphate receptor
- 関
- イノシトール三リン酸受容体、イノシトール3リン酸受容体、イノシトール3リン酸レセプター、イノシトール三リン酸レセプター
「イノシトール三リン酸レセプター」
- 英
- inositol 1,4,5-trisphosphate receptor
- 関
- イノシトール三リン酸受容体、イノシトール1,4,5-三リン酸受容体、イノシトール3リン酸受容体、イノシトール3リン酸レセプター
「イノシトール1,4,5-トリスリン酸受容体」
- 英
- inositol-1,4,5-triphosphate receptors, inositol 1,4,5-trisphosphate receptor,IP3 receptor, IP3R
- 関
- イノシトール三リン酸受容体、IP3受容体
「trisphosphate」
「inositol」