Neurotransmission Alphabetical 28/7/05 15:52 Page 1

Total Page:16

File Type:pdf, Size:1020Kb

Neurotransmission Alphabetical 28/7/05 15:52 Page 1 neuroscience - Neurotransmission alphabetical 28/7/05 15:52 Page 1 Abcam’s range of Neuroscience receptor, channel and ligand antibodies includes over 320 tried and tested products www.abcam.com Neurotransmission - receptor and channel signaling www.abcam.com GPCRs TYROSINE KINASES ION CHANNELS Neurotrophins rin u BDNF rt NGF u NT-3 Glutamate GABA ACh GDNF Ne Artemin Persepin NT-4/5 Glutamate Anandamide ATP Glycine ␥ 2-AG 1 2 3 4 / ␣ ␣ ␣ ␣ R / u A GFR GFR GFR GFR NTR mGL X1, 2, 3 CB1/2 2 EphA/B* Ephrin RET TrkA/B/C p75 AMPA/KainateNMDAR P GABA GlyR nAChR IP3 released Lyn Ephexin Homer DAG Adenylate Fyn PI3K Gr Src PSD95 Rapsin i PD2RGS3 Shc Syntrophin b K PLC Gi/q cyclase Gi 4 NcK PI3 Shc + 2+ 2+ PI3K PLC ␥ Na Ca Ca P PI3K Grb2 PLC␤/␥ PKC nNOS ␥ FAK PiP3/4 SOS MEK CaM Cl- Cl- ER NFkB PDEI PKA Rac RhoA RasGAP Src PTEN PKC Ras GTPase ERK CaMK 2+ PKK2 Calcineurin Ca released ROCK ERK FRS2 AKT/PKB Raf JNK nNOS SynGAP Grb2 actin MEK 1/2 P Ser133 Inhibition Cl- Src SOS Cell survival CREB of signaling RAS P CREB ERK 1/2 P P MAPK GSK3 ELK RSK NF␬B CREB CREB gene Long term Cytoskeleton transcription synaptic dynamics, neurite ASK1 Bad CRE plasticity (LTP) P P extension CREB CREB Short term MKK3/6 Apoptosis plasticity Others Other GPCRs - ARA9 ACh (Muscarinic): M1, M2, M3, M4 CRE p38MAPK c-fos Potassium - ASIC␤, ASIC3 Adrenalin: Alpha1b, 1c, 1d - KChIP2 - DDR 1, 2 ATP: P2Y MSK1 c-j c-fos gene - KCNQ 3, 5 - ENSA Dopamine: D1, D4 u transcription - Kv beta 2 - GJB1 n GABA: GABAB receptor - Kv 1.2 - SLC31A1 ␦ ␬ P P Opioid: µ, , CREB CREB AP1 - Kv 1.3 - TRAR4 Neurotensin: 1, 2 Growth, - Kv 1.4 - TRPM7 Neurokinin: NKA, NKB, NK1, Calcitonin development & Sodium - Kv 2.2 - VR1 * forward/reverse signalling differentation Serotonin: 5HT-1B, D, E, F, 5HT-2A, B, 5HT-3, 4, 6, 7 inhibitory pathway CRE - APXL - Kv 4.2 - VRL1 neuroscience - Neurotransmission alphabetical 28/7/05 15:52 Page 2 Browse our datasheets for the latest customer reviews and enquires on neurotransmission products! www.abcam.com Target Datasheet Clonality Applications Neurotensin Receptor 2 13069 P IHC-P Kv2.2 (azide free) 21909 P IHC, WB www.abcam.com/ab tested NPY5R 13199 P ICC, IHC-P Kv4.2 16719 P IF, IP, WB P Y12 13373 P ICC, IHC-P Cannabinoid & Dopamine 2 more ion channels Cannabinoid Receptor I 10573 P IF, IHC-Fr, WB P2Y2 10270 P IHC-Fr Somatostatin Receptor 2 13120 P IF, IHC-P 5HT3 Receptor 13897 P WB Cannabinoid Receptor II 3560 P ICC, WB alpha 1 Glycine Receptor 475 P IP, WB Dopamine Receptor D1 12969 P ICC, IHC-P Tyrosine Kinases ARA9 [35-2] 468 M WB Dopamine Receptor D4 13318 P IHC-P EphA1 5376 P ELISA, WB DDR1 5508 P ELISA, WB Glutamate EphA2 5386 P ELISA, WB DDR2 5520 P ELISA, WB Homer (1a+1b+1c) 11157 P IHC-Fr, WB EphB1 7042 ELISA, WB KA1 10101 P WB GRM8 13194 P IHC-P EphB2 5418 P ELISA, WB P2X2 10266 P ICC, IHC-Fr, WB mGluR1a 6439 PIF, IHC, IHC-Fr, IP, WB EphB3 10617 P ELISA, WB P2X3 10269 P ICC, IHC-Fr, WB mGluR2 [mG2Na-s] 15672 M IF, IHC, WB Fyn 802 P ELISA, WB TRPM7 729 P WB ␣ mGluR2+3 6438 P IHC, IP, WB GFR 3 19135 P WB Vanilloid Receptor 1 6166 P IF, IHC-Fr, IHC-P Lyn 1959 P IF, IP, WB mGluR3 10309 P WB KEY: M - Monoclonal P - Polyclonal mGluR5 6436 P IHC, IP, WB p75 NTR 10495 P EM, FACS,ICC, IF, IP, WB mGluR7 13363 P IHC-P TrkA 8871 P IF, IHC, IP, trkA inact. WB TrkB 6180 P IHC-Fr Cannabinoid Receptor I antibody (ab10573) Opioid & Seratonin Cannabinoid receptor 1 (CB1) inhibits adenylate cyclase activity in a 5-HT1B 13154 P IHC-P GABA receptors ␣ dose dependent, stereoselective and pertussis toxin sensitive manner. 5HT2B 13292 P IHC-P GABA A Receptor 1 8341 P WB ␣ CB1 also stimulates the mitogen-activated protein kinase and 5HT3 13897 P WB GABA A Receptor 2 8342 P WB modulates ion channels through direct G-protein interactions. ␤ 5-HT4 10095 P WB GABA A Receptor 2 8340 P IP, WB ␦ CB1 is primarily expressed in the brain. 5HT6 13293 P IHC-P GABA A Receptor 10100 P WB ␥ ab10573 shows localisation in neurons Delta Opioid Receptor 10272 P ICC GABA A Receptor 2 4073 P IP, WB GABA B Receptor 2 1134 P WB of the arcuate nucleus of rat brain Kappa Opioid Receptor 10283 P ICC, IHC-Fr hypothalamus (shown here). CB1 is also Mu Opioid Receptor 10275 P ICC, IHC-Fr, WB nAch receptors expressed at low level in peripheral tissues including adrenal, heart, lung, prostate, Neurotrophins nAChR [88B] 2804 M IHC-Fr, IP, WB ␣ uterus, ovary, testis, bone marrow, thymus, Artemin 1136 P WB nAChR [D6] 11149 M FACS, IHC-Fr, IP, WB ␤ and tonsil. BDNF 6201 P ELISA, IHC-Fr, Neut, WB nAChR [B3] 11150 M FACS, IHC-Fr, IP, WB ␥ GDNF 6206 P Dot, IHC-Fr, WB nAChR [C9] 11151 M FACS, IHC-Fr, IP, WB Applications tested for ab10573: Neurturin 6208 P Dot, ELISA, IHC-Fr, WB Rapsyn [1234] 11423 M ICC, IF, IHC-Fr, WB G western blot G immunofluorescence G immunohistochemistry NGF 6198 P ELISA, IHC-Fr, Neut, WB Syntrophin [1351] 11425 M IF, IP, WB Mu Opioid Receptor antibody (ab10275) other GPCRs NMDA receptors NMDAR1 C1 6484 P IHC, IP, WB ␣1d Adrenergic Receptor 12923 P IHC-P Three major opioid receptor families have now been proposed: mu, NMDAR1 [R1JHL] 1880 M WB Calcitonin Receptor 11042 P ELISA, IHC-P, WB kappa and delta. Mu Opioid Receptor (MOR) plays a mandatory role in NMDAR1 N1 6483 P IHC, IP, WB CCKBR 14440 P IHC-P, WB the analgesic effects of opioids and most of the opioid analgesics used NMDAR2A 108 P AF, IHC-F, IHC-Fr, IP, WB Corticotropin R F Receptor 12964 P IF, IHC-Fr, IHC-P, WB clinically today selectively bind to MOR sub types. NMDAR2B 109 P AF, IHC-F, IHC-Fr, IP, WB EDG7 13188 P IHC-P NMDAR2C 110 P IHC, IP, WB MOR is expressed by neurons and glia and GLP1R 13181 P IHC-P is enriched in many brain areas including HRH3 13014 P ICC, IHC-P Sodium and potassium channels cerebral cortex, striatum (shown here MAChR 1 3480 P WB APXL 4948 P Fast track labelled with ab10275), hippocampus, MAChR M3 13064 P IHC-P ASIC3 10354 P ICC, IHC-Fr locus coeruleus and the superficial laminae of the dorsal horn. MC4 Receptor 13034 P ICC, IHC-Fr, IHC-P KChIP2 3473 P WB Melatonin Receptor 1A 13036 P IHC-P KCNQ3 16228 P ICC, IF, IHC-Fr Applications tested for ab10275: Melatonin Receptor 1B 13357 P IHC-P Kv␤2 10665 P ICC, WB G western blot G immunocytochemistry G immunohistochemistry (frozen sections) Neurokinin A Receptor 13397 P ICC, IHC-P Kv1.2 10667 P ICC, WB Neurotensin Receptor 1 13201 P IHC-P Kv1.4 16718 P IF, IP, WB www.abcam.com/neuroscience.
Recommended publications
  • Supporting Information
    Supporting Information Koyanagi et al. 10.1073/pnas.0806215105 SI Materials and Methods CNGB, NM࿝137763; human CNGB1, NM࿝001297; human ࿝ Amino Acid Sequences. The accession numbers of amino acid CNGB3, NM 019098; box jellyfish CNG, AB435552; fruit fly ࿝ ࿝ sequences used for analyses are as follows: Box jellyfish opsin, CNG4, NM 167441; fruit fly CNG3, NM 137871; human ࿝ ࿝ AB435549; sea anemone opsin, BR000662; hydra opsin, Con- CNGA4, NM 001037329; fruit fly CNGA, NM 057768; human CNGA1, NM࿝000087; human CNGA2, NM࿝005140; human tig39347:487820–488855 (http://hydrazome.metazome.net); hy- ࿝ drozaon jellyfish opsin, AB332435; human encephalopsin, CNGA3, NM 001298. AF140242; ragworm c-opsin, AY692353; human rhodopsin, Western Blot Analysis. The proteins extracted from half a rhopalia U49742; human blue, M13299; human red, Z68193; lamprey were separated by 12% SDS/PAGE, transferred onto a PVDF parapinopsin, AB116380; lizard parietopsin, DQ100320; am- membrane, and incubated with 1:500 diluted anti-box jellyfish phioxus peropsin, AB050610; human peropsin, AF012270; hu- opsin antiserum. Visualization was carried out by the ABC man rgr, U15790; squid retinochrome, X57143; human melan- method (Vectastain) and by staining with 3,3Ј-diaminobenzidine opsin, AF147788; amphioxus melanopsin, AB205400; squid (Sigma). rhodopsin, X70498; fruit fly Rh1, K02315; human neuropsin, AY377391; amphioxus rhodopsin, AB050606; scallop Go- In Situ Hybridization. Digoxigenin-labeled antisense and sense RNA rhodopsin, AB006455; human muscarinic acetylcholine receptor probes for the box jellyfish opsin were synthesized by using the DIG M1 (CHRM1), NM࿝000738; human melatonin receptor 1A RNA labeling kit (Roche). Sections were pretreated with protein- (MTNR1A), NM࿝005958; Arabidopsis AKT1, U06745; Arabi- ase K and hybridized with each RNA probe.
    [Show full text]
  • The G Protein-Coupled Receptor Subset of the Dog Genome Is More Similar
    BMC Genomics BioMed Central Research article Open Access The G protein-coupled receptor subset of the dog genome is more similar to that in humans than rodents Tatjana Haitina1, Robert Fredriksson1, Steven M Foord2, Helgi B Schiöth*1 and David E Gloriam*2 Address: 1Department of Neuroscience, Functional Pharmacology, Uppsala University, BMC, Box 593, 751 24, Uppsala, Sweden and 2GlaxoSmithKline Pharmaceuticals, New Frontiers Science Park, 3rd Avenue, Harlow CM19 5AW, UK Email: Tatjana Haitina - [email protected]; Robert Fredriksson - [email protected]; Steven M Foord - [email protected]; Helgi B Schiöth* - [email protected]; David E Gloriam* - [email protected] * Corresponding authors Published: 15 January 2009 Received: 20 August 2008 Accepted: 15 January 2009 BMC Genomics 2009, 10:24 doi:10.1186/1471-2164-10-24 This article is available from: http://www.biomedcentral.com/1471-2164/10/24 © 2009 Haitina et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Background: The dog is an important model organism and it is considered to be closer to humans than rodents regarding metabolism and responses to drugs. The close relationship between humans and dogs over many centuries has lead to the diversity of the canine species, important genetic discoveries and an appreciation of the effects of old age in another species. The superfamily of G protein-coupled receptors (GPCRs) is one of the largest gene families in most mammals and the most exploited in terms of drug discovery.
    [Show full text]
  • Genetic Basis of Idiopathic Scoliosis
    Research & Review: Management of Cardiovascular and Orthopedic Complications Volume 1 Issue 1 Genetic Basis of Idiopathic Scoliosis S. Sreeremya Assistant Professor, Department of Biotechnology, Sree Narayana Guru College, Coimbatore, Tamil Nadu, India Email: [email protected] Abstract Idiopathic scoliosis (IS), the most usual spinal deformity, affects otherwise healthy children and adolescents during growth. The etiology is still not quiet understood, although genetic factors are believed to be important. This review corroborates the understanding of IS as a complex disease with a polygenic background. Presumably IS can be typically due to a spectrum of genetic risk variants, ranging from very rare or even private to very common. The most promising candidate genes are highlighted. Keywords: Idiopathic scoliosis, Genetics, Pathogenesis, Heredity INTRODUCTION marked by phenotypic complexity Idiopathic scoliosis (IS), the most general (variations in curve morphology and form of spinal deformity, affects otherwise magnitude, age of onset, rate of healthy children and adolescents during progression), and a prognosis mainly growth (Fig: 1). It usually presents as a rib ranging from increase in curve magnitude, hump visible at forward bending, together to stabilization, or to resolution with with unlevelled shoulders and an growth [5]. Genetic factors are known to asymmetrical waist [1]. According to play a pivotal role, as observed in twin Cobb, the diagnosis is specifically studies and their observation and singleton confirmed by a standing spinal radiograph multigenerational families [6]. A recent showing a lateral curvature of the spine research of monozygotic and dizygotic exceeding 10° [2]. A main concern in IS is twins from the Swedish twin registry the absence of reliable means by which to estimated that overall genetic effects predict risk of progression, leading to accounted for 39 % of the observed frequent follow-ups, radiographs, and phenotypic variance, leaving the remaining potentially unnecessary brace treatments.
    [Show full text]
  • Expression of Melatonin Receptors 1A/1B, Calmodulin and Estrogen Receptor 2 in Deep Paravertebral Muscles Revisited
    MOLECULAR MEDICINE REPORTS 14: 5719-5724, 2016 Etiopathogenesis of adolescent idiopathic scoliosis: Expression of melatonin receptors 1A/1B, calmodulin and estrogen receptor 2 in deep paravertebral muscles revisited JOSEF ZAMECNIK1*, LENKA KRSKOVA1*, JAROMIR HACEK1, IVANA STETKAROVA2 and MARTIN KRBEC3 1Department of Pathology and Molecular Medicine, 2nd Faculty of Medicine, Charles University in Prague and University Hospital Motol, 15006 Prague; 2Department of Neurology, Charles University; 3Department of Orthopedics and Traumatology, 3rd Faculty of Medicine, Charles University in Prague and University Hospital Královské Vinohrady, 10034 Prague, Czech Republic Received October 28, 2015; Accepted October 11, 2016 DOI: 10.3892/mmr.2016.5927 Abstract. The pathogenesis of adolescent idiopathic scoliosis addition, no difference in expression was detected between the (AIS), including the associated local changes in deep para- patients with AIS and the controls. With regards to MTNR1A vertebral muscles, is poorly understood. The asymmetric and MTNR1B, their expression was very weak in paravertebral expression of several molecules involved in the melatonin muscles, and in the majority of cases their expression could signaling pathway, including melatonin receptors 1A/1B not be detected by repeated RT-qPCR analysis. Therefore, (MTNR1A/MTNR1B), estrogen receptor 2 (ESR2) and these data do not support the previously suggested role of the calmodulin (CALM1), has previously been suggested to be asymmetric expression of molecules involved in the melatonin associated with AIS. However, this hypothesis is based on signaling pathway in deep paravertebral muscles in the patho- single studies in which the data were obtained by different genesis of AIS. methodological approaches. Therefore, to evaluate the symmetry of the mRNA expression levels of these molecules, Introduction 18 patients with AIS and 10 non-scoliotic controls were enrolled in the present study.
    [Show full text]
  • The Neuroprotective Effects of Melatonin: Possible Role in the Pathophysiology of Neuropsychiatric Disease
    brain sciences Perspective The Neuroprotective Effects of Melatonin: Possible Role in the Pathophysiology of Neuropsychiatric Disease Jung Goo Lee 1,2 , Young Sup Woo 3, Sung Woo Park 2,4, Dae-Hyun Seog 5, Mi Kyoung Seo 6 and Won-Myong Bahk 3,* 1 Department of Psychiatry, College of Medicine, Haeundae Paik Hospital, Inje University, Busan 47392, Korea; [email protected] 2 Paik Institute for Clinical Research, Department of Health Science and Technology, Graduate School, Inje University, Busan 47392, Korea; [email protected] 3 Department of Psychiatry, College of Medicine, The Catholic University of Korea, Seoul 07345, Korea; [email protected] 4 Department of Convergence Biomedical Science, College of Medicine, Inje University, Busan 47392, Korea 5 Department of Biochemistry, College of Medicine, Inje University, Busan 47392, Korea; [email protected] 6 Paik Institute for Clinical Research, Inje University, Busan 47392, Korea; [email protected] * Correspondence: [email protected] Received: 16 September 2019; Accepted: 19 October 2019; Published: 21 October 2019 Abstract: Melatonin is a hormone that is secreted by the pineal gland. To date, melatonin is known to regulate the sleep cycle by controlling the circadian rhythm. However, recent advances in neuroscience and molecular biology have led to the discovery of new actions and effects of melatonin. In recent studies, melatonin was shown to have antioxidant activity and, possibly, to affect the development of Alzheimer’s disease (AD). In addition, melatonin has neuroprotective effects and affects neuroplasticity, thus indicating potential antidepressant properties. In the present review, the new functions of melatonin are summarized and a therapeutic target for the development of new drugs based on the mechanism of action of melatonin is proposed.
    [Show full text]
  • Quantigene Flowrna Probe Sets Currently Available
    QuantiGene FlowRNA Probe Sets Currently Available Accession No. Species Symbol Gene Name Catalog No. NM_003452 Human ZNF189 zinc finger protein 189 VA1-10009 NM_000057 Human BLM Bloom syndrome VA1-10010 NM_005269 Human GLI glioma-associated oncogene homolog (zinc finger protein) VA1-10011 NM_002614 Human PDZK1 PDZ domain containing 1 VA1-10015 NM_003225 Human TFF1 Trefoil factor 1 (breast cancer, estrogen-inducible sequence expressed in) VA1-10016 NM_002276 Human KRT19 keratin 19 VA1-10022 NM_002659 Human PLAUR plasminogen activator, urokinase receptor VA1-10025 NM_017669 Human ERCC6L excision repair cross-complementing rodent repair deficiency, complementation group 6-like VA1-10029 NM_017699 Human SIDT1 SID1 transmembrane family, member 1 VA1-10032 NM_000077 Human CDKN2A cyclin-dependent kinase inhibitor 2A (melanoma, p16, inhibits CDK4) VA1-10040 NM_003150 Human STAT3 signal transducer and activator of transcripton 3 (acute-phase response factor) VA1-10046 NM_004707 Human ATG12 ATG12 autophagy related 12 homolog (S. cerevisiae) VA1-10047 NM_000737 Human CGB chorionic gonadotropin, beta polypeptide VA1-10048 NM_001017420 Human ESCO2 establishment of cohesion 1 homolog 2 (S. cerevisiae) VA1-10050 NM_197978 Human HEMGN hemogen VA1-10051 NM_001738 Human CA1 Carbonic anhydrase I VA1-10052 NM_000184 Human HBG2 Hemoglobin, gamma G VA1-10053 NM_005330 Human HBE1 Hemoglobin, epsilon 1 VA1-10054 NR_003367 Human PVT1 Pvt1 oncogene homolog (mouse) VA1-10061 NM_000454 Human SOD1 Superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))
    [Show full text]
  • Genetic Variations of Melatonin Receptor Type 1A Are Associated with the Clinicopathologic Development of Urothelial Cell Carcin
    Int. J. Med. Sci. 2017, Vol. 14 1130 Ivyspring International Publisher International Journal of Medical Sciences 2017; 14(11): 1130-1135. doi: 10.7150/ijms.20629 Research Paper Genetic Variations of Melatonin Receptor Type 1A are Associated with the Clinicopathologic Development of Urothelial Cell Carcinoma Yung-Wei Lin1, 2, Shian-Shiang Wang3, 4, 5, Yu-Ching Wen2, 6, Min-Che Tung1, 7, Liang-Ming Lee2, 6, Shun-Fa Yang5, 8, Ming-Hsien Chien1, 9 1. Graduate Institute of Clinical Medicine, Taipei Medical University, Taipei, Taiwan; 2. Department of Urology, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan; 3. Division of Urology, Department of Surgery, Taichung Veterans General Hospital, Taichung, Taiwan; 4. School of Medicine, Chung Shan Medical University, Taichung, Taiwan; 5. Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan; 6. Department of Urology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan; 7. Department of Surgery, Tungs' Taichung Metro Harbor Hospital, Taichung, Taiwan; 8. Department of Medical Research, Chung Shan Medical University Hospital, Taichung, Taiwan; 9. Department of Medical Education and Research, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan. Corresponding authors: Ming-Hsien Chien, PhD, Graduate Institute of Clinical Medicine, Taipei Medical University, 250 Wu-Hsing Street, Taipei 11031, Taiwan; Phone: 886-2-27361661, ext. 3237; Fax: 886-2-27390500; E-mail: [email protected] or Shun-Fa Yang, PhD, Institute of Medicine, Chung Shan Medical University, 110 Chien-Kuo N. Road, Section 1, Taichung 402, Taiwan; Phone: 886-4-2473959, ext. 34253; Fax: 886-4-24723229; E-mail: [email protected] © Ivyspring International Publisher.
    [Show full text]
  • Neurotransmission: Receptor Signaling
    Neurotransmission - receptor and channel signaling GPCRs TYROSINE KINASES ION CHANNELS Neurotrophins BDNF NGF NT-3 Glutamate GABA ACh GDNF Neurturin Artemin Persepin NT-4/5 Glutamate Anandamide ATP Glycine γ 2 1 4 3 / α α α 2-AG α β / α A GFR GFR GFR GFR NTR mGLuR A/B/C X1, 2, 3 CB1/2 2 EphA/B* Ephrin RET Trk p75 AMPA/KainateNMDAR P GABA GlyR nAChR IP3 Lyn released Ephexin Fyn Rapsin Homer DAG Adenylate PI3K Grb4 Src PSD95 HAP1 Syntrophin i PD Shc Gephyrin Gi/q cyclase Gi K PLC GABARAP NcK 2RGS3 PI3 Shc + 2+ 2+ GRIF1 PI3K PLC γ Na Ca Ca P PI3K Grb2 PLCβ/γ PKC nNOS γ FAK PiP3/4 SOS MEK CaM Cl- Gephyrin Cl- ER NFkB PDEI PKA Rac RhoA RasGAP Src PTEN PKC Ras GTPase ERK CaMK Cl- 2+ PKK2 Calcineurin Ca ROCK ERK FRS2 AKT/PKB released Raf JNK nNOS SynGAP Grb2 actin MEK 1/2 P Ser133 Inhibition Excitation Src SOS Cell survival CREB of signaling of signaling RAS P CREB ERK 1/2 P P MAPK GSK3 ELK RSK NFκB CREB CREB gene Long term Cytoskeleton transcription synaptic dynamics, neurite ASK1 Bad CRE plasticity (LTP) P P extension CREB CREB Short term MKK3/6 Apoptosis plasticity Others Other GPCRs - ARA9 ACh (Muscarinic): M1, M2, M3, M4 CRE p38MAPK c-fos Potassium - ASICβ, ASIC3 Adrenalin: Alpha1b, 1c, 1d - KChIP2 - DDR 1, 2 ATP: P2Y MSK1 c-jun c-fos gene - KCNQ 3, 5 - ENSA Dopamine: D1, D4 transcription - Kv beta 2 - GJB1 GABA: GABAB receptor - Kv 1.2 - SLC31A1 μ δ κ P P Opioid: , , CREB CREB AP1 - Kv 1.3 - TRAR4 Neurotensin: 1, 2 Growth, - Kv 1.4 - TRPM7 Neurokinin: NKA, NKB, NK1, Calcitonin development & Sodium - Kv 2.2 - VR1 * forward/reverse signalling
    [Show full text]
  • The Role of Melatonin in Diabetes: Therapeutic Implications
    review The role of melatonin in diabetes: therapeutic implications Shweta Sharma1, Hemant Singh1, Nabeel Ahmad2, Priyanka Mishra1, Archana Tiwari1 ABSTRACT Melatonin referred as the hormone of darkness is mainly secreted by pineal gland, its levels being 1 School of Biotechnology, Rajiv elevated during night and low during the day. The effects of melatonin on insulin secretion are me- Gandhi Technical University, Gandhi diated through the melatonin receptors (MT1 and MT2). It decreases insulin secretion by inhibiting Nagar, Bhopal, Madhya Pradesh cAMP and cGMP pathways but activates the phospholipaseC/IP3 pathway, which mobilizes Ca2+ from 2 School of Biotechnology, organelles and, consequently increases insulin secretion. Both in vivo and in vitro, insulin secretion IFTM University, Lodhipur Rajput, Uttar Pradesh by the pancreatic islets in a circadian manner, is due to the melatonin action on the melatonin recep- tors inducing a phase shift in the cells. Melatonin may be involved in the genesis of diabetes as a Correspondence to: reduction in melatonin levels and a functional interrelationship between melatonin and insulin was Shweta Sharma School of Biotechnology observed in diabetic patients. Evidences from experimental studies proved that melatonin induces Rajiv Gandhi Technical University production of insulin growth factor and promotes insulin receptor tyrosine phosphorylation. The dis- Airport Bypass Road, Gandhi Nagar turbance of internal circadian system induces glucose intolerance and insulin resistance, which could 462036 – Bhopal, Madhya Pradesh [email protected] be restored by melatonin supplementation. Therefore, the presence of melatonin receptors on hu- man pancreatic islets may have an impact on pharmacotherapy of type 2 diabetes. Arch Endocrinol Metab. Received on June/8/2015 2015;59(5):391-9 Accepted on July/6/2015 DOI: 10.1590/2359-3997000000098 Keywords Melatonin; diabetes; insulin; beta cells; calcium; circadian rhythm INTRODUCTION tomy of rodents causes hyperinsulinemia (7).
    [Show full text]
  • Inflammatory Modulation of Hematopoietic Stem Cells by Magnetic Resonance Imaging
    Electronic Supplementary Material (ESI) for RSC Advances. This journal is © The Royal Society of Chemistry 2014 Inflammatory modulation of hematopoietic stem cells by Magnetic Resonance Imaging (MRI)-detectable nanoparticles Sezin Aday1,2*, Jose Paiva1,2*, Susana Sousa2, Renata S.M. Gomes3, Susana Pedreiro4, Po-Wah So5, Carolyn Ann Carr6, Lowri Cochlin7, Ana Catarina Gomes2, Artur Paiva4, Lino Ferreira1,2 1CNC-Center for Neurosciences and Cell Biology, University of Coimbra, Coimbra, Portugal, 2Biocant, Biotechnology Innovation Center, Cantanhede, Portugal, 3King’s BHF Centre of Excellence, Cardiovascular Proteomics, King’s College London, London, UK, 4Centro de Histocompatibilidade do Centro, Coimbra, Portugal, 5Department of Neuroimaging, Institute of Psychiatry, King's College London, London, UK, 6Cardiac Metabolism Research Group, Department of Physiology, Anatomy & Genetics, University of Oxford, UK, 7PulseTeq Limited, Chobham, Surrey, UK. *These authors contributed equally to this work. #Correspondence to Lino Ferreira ([email protected]). Experimental Section Preparation and characterization of NP210-PFCE. PLGA (Resomers 502 H; 50:50 lactic acid: glycolic acid) (Boehringer Ingelheim) was covalently conjugated to fluoresceinamine (Sigma- Aldrich) according to a protocol reported elsewhere1. NPs were prepared by dissolving PLGA (100 mg) in a solution of propylene carbonate (5 mL, Sigma). PLGA solution was mixed with perfluoro- 15-crown-5-ether (PFCE) (178 mg) (Fluorochem, UK) dissolved in trifluoroethanol (1 mL, Sigma). This solution was then added to a PVA solution (10 mL, 1% w/v in water) dropwise and stirred for 3 h. The NPs were then transferred to a dialysis membrane and dialysed (MWCO of 50 kDa, Spectrum Labs) against distilled water before freeze-drying. Then, NPs were coated with protamine sulfate (PS).
    [Show full text]
  • The Dominant Somatostatin Receptor in Neuroendocrine Tumors of North Indian Population 1Narendra Krishnani, 2Niraj Kumari, 3Rajneesh K Singh, 4Pooja Shukla
    WJOES Narendra Krishnani et al 10.5005/jp-journals-10002-1171 ORIGINAL ARTICLE The Dominant Somatostatin Receptor in Neuroendocrine Tumors of North Indian Population 1Narendra Krishnani, 2Niraj Kumari, 3Rajneesh K Singh, 4Pooja Shukla ABSTRACT Neuroendocrine Tumors of North Indian Population. World J Endoc Surg 2015;7(3):60-64. Introduction: Neuroendocrine tumors (NET) express diffe­ rent types of somatostatin receptors (SSTRs) that bind to syn­ Source of support: Nil thetic analogs with variable affinity. It is important to know the Conflict of interest: None expression profile of SSTRs to predict biological effect of somato- statin analogues. We studied SSTR2 and SSTR5 expre ssion by immunohistochemistry (IHC) to assess the dominant sub­ INTRODUCTION type in NETs and correlate the expression with histological Neuroendocrine tumors (NET) are heterogeneous group prognostic parameters. of neoplasms that arise primarily in gastrointestinal tract Materials and methods: Fifty­three consecutive cases of NET (GIT), pancreas and lung.1 Ninety percent of these tumors from all sites were evaluated for SSTR2 and SSTR5 expres­ are nonfunctional, that is, they do not produce bio- sion by IHC. The expression was correlated with histological features of NETs. logically active peptides but are diagnosed late because of their mass effect.2 A common feature of all NETs is Results: Forty­four cases were resected specimens and 9 were small biopsies. Nine of 53 cases (16.9%) were functional expression of different types of somatostatin receptors tumors. There were 24 NETs from gastrointestinal tract (GIT), (SSTRs) which are seen in approximately 80 to 90% of 19 from pancreas and 10 from miscellaneous sites.
    [Show full text]
  • Supplementary Table 2
    Supplementary Table 2. Differentially Expressed Genes following Sham treatment relative to Untreated Controls Fold Change Accession Name Symbol 3 h 12 h NM_013121 CD28 antigen Cd28 12.82 BG665360 FMS-like tyrosine kinase 1 Flt1 9.63 NM_012701 Adrenergic receptor, beta 1 Adrb1 8.24 0.46 U20796 Nuclear receptor subfamily 1, group D, member 2 Nr1d2 7.22 NM_017116 Calpain 2 Capn2 6.41 BE097282 Guanine nucleotide binding protein, alpha 12 Gna12 6.21 NM_053328 Basic helix-loop-helix domain containing, class B2 Bhlhb2 5.79 NM_053831 Guanylate cyclase 2f Gucy2f 5.71 AW251703 Tumor necrosis factor receptor superfamily, member 12a Tnfrsf12a 5.57 NM_021691 Twist homolog 2 (Drosophila) Twist2 5.42 NM_133550 Fc receptor, IgE, low affinity II, alpha polypeptide Fcer2a 4.93 NM_031120 Signal sequence receptor, gamma Ssr3 4.84 NM_053544 Secreted frizzled-related protein 4 Sfrp4 4.73 NM_053910 Pleckstrin homology, Sec7 and coiled/coil domains 1 Pscd1 4.69 BE113233 Suppressor of cytokine signaling 2 Socs2 4.68 NM_053949 Potassium voltage-gated channel, subfamily H (eag- Kcnh2 4.60 related), member 2 NM_017305 Glutamate cysteine ligase, modifier subunit Gclm 4.59 NM_017309 Protein phospatase 3, regulatory subunit B, alpha Ppp3r1 4.54 isoform,type 1 NM_012765 5-hydroxytryptamine (serotonin) receptor 2C Htr2c 4.46 NM_017218 V-erb-b2 erythroblastic leukemia viral oncogene homolog Erbb3 4.42 3 (avian) AW918369 Zinc finger protein 191 Zfp191 4.38 NM_031034 Guanine nucleotide binding protein, alpha 12 Gna12 4.38 NM_017020 Interleukin 6 receptor Il6r 4.37 AJ002942
    [Show full text]