DOCSLIB.ORG

IHC‐Plustm Nb Bod

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
IHC‐Plustm Nb Bod May 2011 Catalog IHC‐plusTM Anbodies …..because seeing is believing. IHC-plus™ Antibodies ...because seeing is believing! LSBio is the world's largest supplier of Immunohistochemistry (IHC) antibodies with more than 27,000 having been tested and approved for use in IHC. More than 4,500 of these antibodies have been further validated specifically for use under LSBio's standardized IHC conditions against formalin-fixed paraffin-embedded human tissues. These are LSBio's premier IHC-plus™ brand antibodies. Visit ww.lsbio.com to learn more about our IHC validation procedure or for the most up to data list of IHC-plusTM antibodies. Host/Reactivity Application CD44 Antigen (CD44) Synaptophysin (SYP) Caspase 3 (CASP3) LS-B1862, IHC, Human skin LS-B3393, IHC, Human adrenal LS-B3404, IHC, Human spleen Clonality Solute Carrier Family 5 (sodium/glucose Histone Deacetylase 1 (HDAC1) ATP-Binding Cassette, Sub-Family B (Mdr/Tap), Cotransporter), Member 10 (SLC5A10) LS-B3438, IHC, Human colon Member 1 (Abcb1) LS-A2800, IHC, Human skeletal muscle LS-B1448, IHC, Human kidney Cyclin D1 (CCND1) Integrin, Alpha X (Antigen CD11C (P150), Alpha Transient Receptor Potential Cation Channel, LS-B3452, IHC, Human testis Polypeptide) (ITGAX) Subfamily A, Member 1 (TRPA1) LS-A9382, IHC, Human tonsil LS-A9098, IHC, Human dorsal root ganglia Host/Species Reactivity Abbreviation Species Av Avian Ba Baboon Bo Bovine Ca Cat Ch Chimpanzee Ck Chicken Do Dog Dr Drosophila Ec E. coli Fe Ferret Fi Atlantic salmon Fr Frog Gp Guinea Pig Gt Goat Ha Hamster Ho Horse Hu Human Ma Mammal Mo Monkey Mu Mouse Op Opossum Po Porcine Pr Primate Rb Rabbit Rt Rat Sp Sheep Ys Yeast Zf Zebrafish Applications Abbreviation Application IHC-P Immunohistochemistry Paraffin IHC-F Immunohistochemistry Frozen WB Western Blot IP Immunoprecipitation IF Immunofluorescence Flo Flow Cytometry Clonality Abbreviation Type M Monoclonal P Polyclonal Catalog Target Name Host Type Reactivity Application LS-B2967 14-3-3 Protein Tau (YWHAQ) Mo M Hu IHC-P, WB LS-B315 53BP1 (TP53BP1) Rb P Hu, Mo IHC-P, WB, other LS-B1714 53BP1 (TP53BP1) Rb P Hu IHC-P, WB LS-B970 5-HT1A Receptor (HTR1A) Rb P Hu IHC-P, WB LS-A586 5-HT1B Receptor (HTR1B) Rb P Hu IHC-P LS-B2041 5-HT1D Receptor (HTR1D) Rb P Hu, Mo IHC-P, WB LS-A6374 5-HT1E Receptor (HTR1E) Rb P Hu IHC-P LS-B4082 5-HT2C Receptor (HTR2C) Rb P Hu IHC-P, WB LS-B971 5-HT3B Receptor (HTR3B) Rb P Hu IHC-P, WB LS-A2118 5-HT5A Receptor (HTR5A) Rb P Hu IHC-P LS-A2119 5-HT5A Receptor (HTR5A) Rb P Hu IHC-P LS-A6693 5-HT5A Receptor (HTR5A) Rb P Hu IHC-P LS-B3428 5-Nucleotidase (NT5E) Rb P Hu, Mo IHC-P, WB LS-B3897 5-Nucleotidase (NT5E) Mo M Hu IHC-P LS-B2943 5-Nucleotidase (NT5E) Mo M Hu IHC-P, WB LS-B1507 A1BG Rb P Hu IHC-P, WB LS-B4153 A1BG Mo M Hu IHC-P, WB LS-A9490 AADAT Rb P Hu IHC-P LS-A9495 AADAT Rb P Hu IHC-P LS-B3833 AAK1 Rb P Hu, Mo, Rt IHC-P, WB LS-B3843 AAK1 Rb P Hu, Mo, Rt IHC-P, WB, other LS-B438 AATF Rb P Hu, Mo IHC-P, WB LS-B2384 ABCA1 Mo M Hu, Mo IHC-P, WB LS-B3038 ABCA1 Rb P Hu, Mo, Rt IHC-P, WB, other LS-B3554 ABCA5 Rb P Hu IHC-P, WB LS-B222 ABCA7 Rat M Mo IHC-P, WB, other LS-B2170 ABCB11 Mo M Hu IHC-P, WB, other LS-B4112 ABCB4 Gt P Hu IHC-P LS-B3454 ABCB5 Rb P Hu IHC-P, WB, other LS-B791 ABCB7 Rb P Hu IHC-P LS-B2746 ABCB9 Gt P Hu IHC-P LS-B2678 ABCC4 Rb P Hu IHC-P, IHC, WB LS-B4 ABCC4 Gt P Hu IHC-P LS-B2334 ABCC5 Gt P Hu, Mo, Rt, other IHC-P, WB LS-B4375 ABCD4 Gt P Hu, Mo, Rt WB LS-B507 ABCG1 Rb P Hu, Mo IHC-P, WB LS-B3788 ABCG2 Mo M Hu IHC-P, other LS-B2767 ABHD4 Gt P Hu, Mo IHC-P LS-B4458 Abhd5 Gt P Hu, Mo, Rt WB LS-B3990 Abhd5 Rb P Hu, Mo, Rt IHC-P, WB LS-B3228 ABTB1 Gt P Hu, Mo IHC-P, WB LS-B4015 ACAA1 Rb P Hu, Rt IHC-P, WB LS-B1500 ACADM Rb P Hu, Mo, other IHC-P, WB LS-B2993 ACADM Gt P Hu IHC-P, WB LS-B4087 ACADS Rb P Hu IHC-P, WB LS-B156 ACCN1 Rb P Hu IHC-P, WB LS-B920 ACCN4 Rb P Hu, Mo, Rt IHC-P, WB LS-B2558 ACE Mo M Hu, Mo, Rt, other IHC-P, WB LS-B3197 ACE2 Rb P Hu IHC-P, WB LS-B439 ACE2 Rb P Hu, Mo IHC-P, WB LS-B3196 ACE2 Rb P Hu IHC-P, WB LS-B1819 Acetylcholinesterase (ACHE) Rb P Hu IHC-P, WB LS-B3190 Acinus (ACIN1) Rb P Hu, Mo IHC-P, WB, other LS-B3189 Acinus (ACIN1) Rb P Hu IHC-P, WB, other LS-B224 Acinus (ACIN1) Rb P Hu IHC-P, WB LS-B3427 ACO2 Rb P Hu, Mo, Rt IHC-P, WB LS-B2961 ACOT11 Mo M Hu IHC-P, WB LS-B4522 ACOT9 Mo M Hu IHC-P, WB, other LS-B2298 ACP2 Gt P Hu, Mo, Rt IHC-P LS-B3108 ACPP Mo M Hu IHC-P LS-B1820 ACSL3 Rb P Hu IHC-P, WB LS-B4440 ACSL4 Gt P Hu, Mo, Rt WB LS-B2761 ACSL5 Gt P Hu IHC-P, WB LS-B4203 ACTA1 Rb P Hu, other IHC-P, WB LS-B3339 ACTA1 Rb P Hu, Rt, other IHC-P LS-B2506 ACTA2 Rb P Hu, Mo, Rt, other IHC-P LS-B2161 ACTA2 Rb P Hu, Mo, Rt, other IHC-P, WB LS-B1039 ACTA2 Rb P Hu IHC-P Page 1 Catalog Target Name Host Type Reactivity Application LS-B3933 ACTA2 Gt P Hu, Mo, Rt IHC-P, WB LS-B4074 ACTA2 Rb P Hu, Mo IHC-P, WB LS-B2847 ACTA2 Mo M Hu, Mo, Rt, other IHC-P, IHC-F, other LS-B3335 ACTH Rb P Hu IHC-P LS-B2977 ACTH Mo M Hu, Rt IHC-P LS-B4067 Activin Type 2 Receptor Rb P Hu IHC-P, WB LS-B4217 ACTN2 Rb P Hu, Mo IHC-P, WB, other LS-B2753 ACTR1B Gt P Hu, Mo, Rt IHC-P, WB LS-B4221 ACTR2 Rb P Hu IHC-P, WB LS-B2695 ACVR1 Rb P Hu, Mo IHC-P, WB LS-B2010 ACVR1 Rb P Hu, Mo, Rt IHC-P, WB LS-B3109 ACVR1 Rb P Hu, Mo, Rt IHC-P, WB LS-B3020 ACVR1 Gt P Hu, Mo, Rt IHC-P, WB LS-B2765 ACYP1 Gt P Hu, Mo, Rt IHC-P, WB LS-B792 ADA Rb P Hu IHC-P LS-B324 ADAM10 Rb P Hu, Mo, Rt IHC-P, WB, other LS-B2756 ADAM12 Gt P Hu IHC-P, WB LS-B4207 ADAM15 Rb P Hu, Mo IHC-P, WB LS-B4068 ADAM8 Rb P Hu IHC-P, WB LS-A1642 ADAMTS1 Rb P Hu IHC-P LS-A1639 ADAMTS1 Rb P Hu IHC-P LS-A1643 ADAMTS1 Rb P Hu IHC-P LS-A1638 ADAMTS1 Rb P Hu IHC-P LS-B4548 ADAMTS17 Mo M Hu, Mo IHC-P, WB LS-A1551 ADAMTS4 Rb P Hu IHC-P LS-A1549 ADAMTS4 Rb P Hu IHC-P LS-A1550 ADAMTS4 Rb P Hu IHC-P LS-A1534 ADAMTS5 Rb P Hu IHC-P LS-B1943 ADD1 Rb P Hu IHC-P, WB LS-B1167 ADD1 Rb P Hu, Mo, Rt IHC-P, WB LS-B3121 ADFP Rb P Hu, Mo, other IHC-P, WB LS-B2168 ADFP Mo M Hu, Rt IHC-P, IHC-F, other LS-B440 Adiponectin (ADIPOQ) Rb P Hu, Mo, Rt IHC-P, WB LS-B2324 Adiponectin Receptor (ADIPOR1) Gt P Hu IHC-P, WB LS-B15 Adiponectin Receptor (ADIPOR1) Rb P Hu IHC-P, WB LS-B125 ADIPOR2 Rb P Hu IHC-P, other LS-B61 ADNP Rb P Hu IHC-P, WB LS-B2122 ADORA2A Mo M Hu, Mo, Rt, other IHC-P, WB, other LS-B3067 ADORA2A Rb P Hu IHC-P, WB, other LS-A680 ADORA2B Rb P Hu IHC-P LS-A699 ADRA1B Rb P Hu IHC-P LS-A696 ADRA1B Rb P Hu IHC-P LS-B1326 AES Rb P Hu, Mo IHC-P, WB, other LS-B441 AES Rb P Hu, Mo, Rt IHC-P, WB, other LS-B796 AFF1 Rb P Hu IHC-P LS-B338 AGAP2 Rb P Hu, Mo, Rt IHC-P, WB, other LS-B4387 AGAP2 Gt P Hu WB LS-B134 AGAP2 Rb P Hu, Mo IHC-P, WB LS-B226 AGGF1 Rb P Hu IHC-P, WB LS-A1561 Aggrecan (ACAN) Rb P Hu IHC-P LS-A1556 Aggrecan (ACAN) Rb P Hu IHC-P LS-B2305 AGPAT6 Rb P Hu, Mo IHC-P, WB LS-B4204 AGPS Rb P Hu, Mo IHC-P, WB LS-B2011 AGR2 Rb P Hu IHC-P LS-B3580 AGR2 Gt P Hu, Mo IHC-P, WB LS-B4510 AGR3 Mo M Hu IHC-P, IHC-F, IHC, WB, other LS-A1322 AGTR2 Rb P Hu IHC-P LS-B4187 AGXT Mo M Hu IHC-P LS-A3391 AH Receptor (AHR) Rb P Hu IHC-P LS-A3017 AH Receptor (AHR) Rb P Hu IHC-P LS-A3005 AH Receptor (AHR) Rb P Hu IHC-P LS-B164 AH Receptor (AHR) Rb P Hu, Mo IHC-P, WB LS-A3018 AH Receptor (AHR) Rb P Hu IHC-P LS-B343 AHSG Gt P Hu IHC-P, WB, other LS-B16 AID (AICDA) Rb P Hu, Mo IHC-P, WB, other LS-B620 AIFM1 Rb P Hu IHC-P, WB LS-B3765 AIFM1 Rb P Hu, Mo, Rt IHC-P, WB, other LS-B699 AIFM1 Rb P Hu, Mo, Rt IHC-P, WB Page 2 Catalog Target Name Host Type Reactivity Application LS-B3744 AIFM1 Rb P Hu IHC-P, WB, other LS-B1508 AIFM1 Rb P Hu, Mo, Rt IHC-P, WB LS-B229 AIFM2 Rb P Hu IHC-P, WB LS-B3000 AIFM2 Gt P Hu IHC-P LS-B2733 AIFM3 Rb P Hu, Mo, Rt IHC-P, WB LS-B3854 AIPL1 Rb P Hu, Mo, Rt IHC-P, WB LS-B3848 AIPL1 Rb P Hu, Mo IHC-P, WB LS-B1741 AIRE Gt P Hu, Rt IHC-P, WB LS-B1740 AIRE Gt P Hu IHC-P, other LS-B4498 AKAP13 Mo M Hu, Rt IHC-P, WB LS-B1509 AKAP7 Rb P Hu IHC-P, WB LS-B3809 AKIRIN1 Rb P Hu, Mo, Rt IHC-P, WB LS-B3810 AKIRIN1 Rb P Hu, Mo, Rt IHC-P, WB LS-B3831 Akirin2 Rb P Hu, Mo, Rt IHC-P, WB LS-B2745 AKR1A1 Gt P Hu, Mo, Rt IHC-P, WB LS-B2012 AKR1B10 Rb P Hu, Mo, Rt IHC-P, WB LS-B4531 AKR1B10 Mo M Hu IHC-P, WB, other LS-B2295 AKR1C3 Gt P Hu IHC-P, WB LS-B2759 AKR1C4 Gt P Hu IHC-P, WB LS-B1663 AKT1 Rb P Hu IHC-P, WB LS-B1183 AKT1 Rb P Hu IHC-P, WB LS-B1168 AKT1 Rb P Hu, Mo, Rt IHC-P, WB LS-B1327 AKT1 Rb P Hu, Mo, Rt IHC-P, WB LS-B1510 AKT1 Rb P Hu, Mo IHC-P, WB LS-B1190 AKT1 Rb P Hu IHC-P, WB LS-B3688 AKT1/2 Rb P Hu, Mo, Rt IHC-P, WB, other LS-B2844 AKT1/2/3 Rb P Hu IHC-P, WB, other LS-B1041 AKT2 Rb P Hu, Mo, Rt IHC-P, WB, other LS-B1320 AKT2 Mo M Hu IHC-P, WB LS-B4129 AKT2 Mo M Hu, Rt IHC-P, WB, other LS-B1169 AKT2 Rb P Hu, Mo, Rt IHC-P, WB LS-B1042 AKT3 Rb P Hu, Mo IHC-P, WB LS-B1319 AKT3 Mo M Hu, Mo, Rt IHC-P, WB LS-B3935 AKT3 Gt P Hu, Mo, Rt, other IHC-P, WB LS-B2013 Alas1 Rb P Hu IHC-P, WB LS-B1855 Albumin (ALB) Mo M Hu IHC-P, WB, other LS-B3900 Albumin (ALB) Mo M Hu IHC-P, WB LS-B325 Albumin (ALB) Rb P Hu IHC-P, WB LS-B3882 ALCAM Mo M Hu IHC-P, WB LS-B3883 ALCAM Mo M Hu IHC-P LS-B2975 ALDH1A1 Rb P Hu IHC-P, WB, other LS-B2497 ALDH1A1 Gt P Hu, Mo, Rt IHC-P, WB LS-B3390 ALDH2 Rb P Hu IHC-P, WB LS-B3807 ALDH3A1 Rb P Hu, Mo, Rt IHC-P, WB LS-B4165 ALDH5A1 Rb P Hu, Mo, Rt IHC-P, WB LS-B1461 ALDOA Gt P Hu IHC-P, WB, other LS-B3453 ALDOC Rb P Hu, Mo IHC-P, WB LS-B1587 ALOX12 Rb P Hu, other IHC-P, WB LS-B4278 ALOX15 Mo M Hu IHC-P, WB LS-B1588 ALOX15B Rb P Hu IHC-P, WB LS-B1499 ALOX5 Rb P Hu, Mo, Rt, other IHC-P, WB, other LS-B2144 ALOX5 Rb P Hu IHC-P, WB LS-B2164 ALOX5 Rb P Hu IHC-P, WB LS-B4240 Alpha 1 Antitrypsin (SERPINA1) Ch P Hu IHC-P, WB LS-B3128 Alpha 1 Antitrypsin (SERPINA1) Mo M Hu IHC-P LS-B1454 Alpha 1 Antitrypsin
Load more

Recommended publications
  • Edinburgh Research Explorer
    Edinburgh Research Explorer International Union of Basic and Clinical Pharmacology. LXXXVIII. G protein-coupled receptor list Citation for published version: Davenport, AP, Alexander, SPH, Sharman, JL, Pawson, AJ, Benson, HE, Monaghan, AE, Liew, WC, Mpamhanga, CP, Bonner, TI, Neubig, RR, Pin, JP, Spedding, M & Harmar, AJ 2013, 'International Union of Basic and Clinical Pharmacology. LXXXVIII. G protein-coupled receptor list: recommendations for new pairings with cognate ligands', Pharmacological reviews, vol. 65, no. 3, pp. 967-86. https://doi.org/10.1124/pr.112.007179 Digital Object Identifier (DOI): 10.1124/pr.112.007179 Link: Link to publication record in Edinburgh Research Explorer Document Version: Publisher's PDF, also known as Version of record Published In: Pharmacological reviews Publisher Rights Statement: U.S. Government work not protected by U.S. copyright General rights Copyright for the publications made accessible via the Edinburgh Research Explorer is retained by the author(s) and / or other copyright owners and it is a condition of accessing these publications that users recognise and abide by the legal requirements associated with these rights. Take down policy The University of Edinburgh has made every reasonable effort to ensure that Edinburgh Research Explorer content complies with UK legislation. If you believe that the public display of this file breaches copyright please contact [email protected] providing details, and we will remove access to the work immediately and investigate your claim. Download date: 02. Oct. 2021 1521-0081/65/3/967–986$25.00 http://dx.doi.org/10.1124/pr.112.007179 PHARMACOLOGICAL REVIEWS Pharmacol Rev 65:967–986, July 2013 U.S.
    [Show full text]
  • Supplementary Data
    Supplemental Data A novel mouse model of X-linked nephrogenic diabetes insipidus: Phenotypic analysis and therapeutic implications Jian Hua Li, Chung-Lin Chou, Bo Li, Oksana Gavrilova, Christoph Eisner, Jürgen Schnermann, Stasia A. Anderson, Chu-Xia Deng, Mark A. Knepper, and Jürgen Wess Supplemental Methods Metabolic cage studies. Animals were maintained in mouse metabolic cages (Hatteras Instruments, Cary, NC) under controlled temperature and light conditions (12 hr light and dark cycles). Mice received a fixed daily ration of 6.5 g of gelled diet per 20 g of body weight per day. The gelled diet was composed of 4 g of Basal Diet 5755 (Test Diet, Richmond, IN), 2.5 ml of deionized water, and 65 mg agar. Preweighted drinking water was provided ad libitum during the course of the study. Mice were acclimated in the metabolic cages for 1-2 days. Urine was collected under mineral oil in preweighted collection vials for successive 24 hr periods. Analysis of GPCR expression in mouse IMCD cells via TaqMan real-time qRT-PCR. Total RNA prepared from mouse IMCD tubule suspensions was reverse transcribed as described under Experimental Procedures. Tissues from ten 10-week old C57BL/6 WT mice were collected and pooled for each individual experiment. cDNA derived from 640 ng of RNA was mixed with an equal volume of TaqMan gene expression 2 x master mix (Applied Biosystems, Foster City, CA). 100 μl-aliquots of this mixture (corresponding to 80 ng of RNA) were added to each of the 8 fill ports of a 384-well plate of a mouse GPCR array panel (Applied Biosystems).
    [Show full text]
  • WO 2019/067413 Al 04 April 2019 (04.04.2019) W 1P O PCT
    (12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date WO 2019/067413 Al 04 April 2019 (04.04.2019) W 1P O PCT (51) International Patent Classification: 16/139,608 24 September 2018 (24.09.2018) US A61K 31/137 (2006.01) A61K 45/06 (2006.01) 16/139,617 24 September 2018 (24.09.2018) US A61P 25/08 (2006.01) 16/139,698 24 September 2018 (24.09.2018) US 16/139,701 24 September 2018 (24.09.2018) US (21) International Application Number: 16/139,704 24 September 2018 (24.09.2018) US PCT/US2018/052580 16/139,763 24 September 2018 (24.09.2018) US (22) International Filing Date: (71) Applicant: ZOGENIX INTERNATIONAL LIMITED 25 September 2018 (25.09.2018) [GB/GB]; Siena Court Broadway, Maidenhead Berkshire (25) Filing Language: English SL6 1NJ (GB). (26) Publication Language: English (72) Inventors; and (71) Applicants: FARFEL, Gail [US/US]; c/o Zogenix, Inc., (30) 5858 Horton Street, Suite 455, Emeryville, California 94608 26 September 2017 (26.09.2017) US (US). LOCK, Michael [US/US]; c/o Zogenix, Inc., 5858 27 September 2017 (27.09.2017) US Horton Street, Suite 455, Emeryville, California 94608 31 October 2017 (3 1. 10.2017) US (US). GALER, Bradley S. [US/US]; 1740 Lenape Road, 30 November 2017 (30. 11.2017) US West Chester, Pennsylvania 19382 (US). MORRISON, 07 February 2018 (07.02.2018) US Glenn [CA/US]; c/o Zogenix, Inc., 5858 Horton Street, 10 May 2018 (10.05.2018) US Suite 455, Emeryville, California 94608 (US).
    [Show full text]
  • A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
    Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated.
    [Show full text]
  • Reck and Gpr124 Activate Canonical Wnt Signaling To
    RECK AND GPR124 ACTIVATE CANONICAL WNT SIGNALING TO CONTROL MAMMALIAN CENTRAL NERVOUS SYSTEM ANGIOGENESIS AND BLOOD-BRAIN BARRIER REGULATION by Chris Moonho Cho A dissertation submitted to Johns Hopkins University in conformity with the requirements for the degree of Doctor of Philosophy Baltimore, Maryland July 2018 © Chris Moonho Cho 2018 All rights reserved Abstract Canonical Wnt signaling plays a pivotal role in promoting central nervous system (CNS) angiogenesis and blood-brain barrier (BBB) formation and maintenance. Specifically, Wnt7a and Wnt7b are required for vascular development in the forebrain and ventral spinal cord. Yet, how these two ligands – among the 19 mammalian Wnts – are selectively communicated to Frizzled receptors expressed on endothelial cells (ECs) remains largely unclear. In this thesis, we propose a novel paradigm for Wnt specificity. We have identified two EC surface proteins – orphan receptor Gpr124, and more recently, GPI-anchored Reck (reversion-inducing cysteine-rich protein with Kazal motifs) – as essential receptor co-factors that assemble into a multi-protein complex with Wnt7a/7b and Frizzled for the development of the mammalian neurovasculature. Specifically, we show that EC-specific reduction in Reck impairs CNS angiogenesis and that EC-specific postnatal loss of Reck, combined with loss of Norrin, impairs BBB maintenance. We identify the critical domains of both Reck and Gpr124 that are required for Wnt activity, and demonstrate that these regions are important for ii direct binding and complex formation. Importantly, weakening this interaction by targeted mutagenesis reduces Reck-Gpr124 stimulation of Wnt7a signaling in cell culture and impairs CNS angiogenesis. Finally, a soluble Gpr124 probe binds specifically to cells expressing Frizzled (Fz), Wnt7a or Wnt7b, and Reck; and a soluble Reck probe binds specifically to cells expressing Fz, Wnt7a or Wnt7b, and Gpr124.
    [Show full text]
  • N-Glycan Trimming in the ER and Calnexin/Calreticulin Cycle
    Neurotransmitter receptorsGABA and A postsynapticreceptor activation signal transmission Ligand-gated ion channel transport GABAGABA Areceptor receptor alpha-5 alpha-1/beta-1/gamma-2 subunit GABA A receptor alpha-2/beta-2/gamma-2GABA receptor alpha-4 subunit GABAGABA receptor A receptor beta-3 subunitalpha-6/beta-2/gamma-2 GABA-AGABA receptor; A receptor alpha-1/beta-2/gamma-2GABA receptoralpha-3/beta-2/gamma-2 alpha-3 subunit GABA-A GABAreceptor; receptor benzodiazepine alpha-6 subunit site GABA-AGABA-A receptor; receptor; GABA-A anion site channel (alpha1/beta2 interface) GABA-A receptor;GABA alpha-6/beta-3/gamma-2 receptor beta-2 subunit GABAGABA receptorGABA-A receptor alpha-2receptor; alpha-1 subunit agonist subunit GABA site Serotonin 3a (5-HT3a) receptor GABA receptorGABA-C rho-1 subunitreceptor GlycineSerotonin receptor subunit3 (5-HT3) alpha-1 receptor GABA receptor rho-2 subunit GlycineGlycine receptor receptor subunit subunit alpha-2 alpha-3 Ca2+ activated K+ channels Metabolism of ingested SeMet, Sec, MeSec into H2Se SmallIntermediateSmall conductance conductance conductance calcium-activated calcium-activated calcium-activated potassium potassium potassiumchannel channel protein channel protein 2 protein 1 4 Small conductance calcium-activatedCalcium-activated potassium potassium channel alpha/beta channel 1 protein 3 Calcium-activated potassiumHistamine channel subunit alpha-1 N-methyltransferase Neuraminidase Pyrimidine biosynthesis Nicotinamide N-methyltransferase Adenosylhomocysteinase PolymerasePolymeraseHistidine basic
    [Show full text]
  • G Protein-Coupled Receptors in Stem Cell Maintenance and Somatic Reprogramming to Pluripotent Or Cancer Stem Cells
    BMB Reports - Manuscript Submission Manuscript Draft Manuscript Number: BMB-14-250 Title: G protein-coupled receptors in stem cell maintenance and somatic reprogramming to pluripotent or cancer stem cells Article Type: Mini Review Keywords: G protein-coupled receptors; stem cell maintenance; somatic reprogramming; cancer stem cells; pluripotent stem cell Corresponding Author: Ssang-Goo Cho Authors: Ssang-Goo Cho1,*, Hye Yeon Choi1, Subbroto Kumar Saha1, Kyeongseok Kim1, Sangsu Kim1, Gwang-Mo Yang1, BongWoo Kim1, Jin-hoi Kim1 Institution: 1Department of Animal Biotechnology, Animal Resources Research Center, and Incurable Disease Animal Model and Stem Cell Institute (IDASI), Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul 143-701, Republic of Korea, UNCORRECTED PROOF 1 G protein-coupled receptors in stem cell maintenance and somatic reprogramming to 2 pluripotent or cancer stem cells 3 4 Hye Yeon Choi, Subbroto Kumar Saha, Kyeongseok Kim, Sangsu Kim, Gwang-Mo 5 Yang, BongWoo Kim, Jin-hoi Kim, and Ssang-Goo Cho 6 7 Department of Animal Biotechnology, Animal Resources Research Center, and 8 Incurable Disease Animal Model and Stem Cell Institute (IDASI), Konkuk University, 9 120 Neungdong-ro, Gwangjin-gu, Seoul 143-701, Republic of Korea 10 * 11 Address correspondence to Ssang-Goo Cho, Department of Animal Biotechnology and 12 Animal Resources Research Center. Konkuk University, 120 Neungdong-ro, Gwangjin- 13 gu, Seoul 143-701, Republic of Korea. Tel: 82-2-450-4207, Fax: 82-2-450-1044, E-mail: 14 [email protected] 15 16 17 18 19 1 UNCORRECTED PROOF 20 Abstract 21 The G protein-coupled receptors (GPCRs) compose the third largest gene family in the 22 human genome, representing more than 800 distinct genes and 3–5% of the human genome.
    [Show full text]
  • Technical Note, Appendix: an Analysis of Blood Processing Methods to Prepare Samples for Genechip® Expression Profiling (Pdf, 1
    Appendix 1: Signature genes for different blood cell types. Blood Cell Type Source Probe Set Description Symbol Blood Cell Type Source Probe Set Description Symbol Fraction ID Fraction ID Mono- Lympho- GSK 203547_at CD4 antigen (p55) CD4 Whitney et al. 209813_x_at T cell receptor TRG nuclear cytes gamma locus cells Whitney et al. 209995_s_at T-cell leukemia/ TCL1A Whitney et al. 203104_at colony stimulating CSF1R lymphoma 1A factor 1 receptor, Whitney et al. 210164_at granzyme B GZMB formerly McDonough (granzyme 2, feline sarcoma viral cytotoxic T-lymphocyte- (v-fms) oncogene associated serine homolog esterase 1) Whitney et al. 203290_at major histocompatibility HLA-DQA1 Whitney et al. 210321_at similar to granzyme B CTLA1 complex, class II, (granzyme 2, cytotoxic DQ alpha 1 T-lymphocyte-associated Whitney et al. 203413_at NEL-like 2 (chicken) NELL2 serine esterase 1) Whitney et al. 203828_s_at natural killer cell NK4 (H. sapiens) transcript 4 Whitney et al. 212827_at immunoglobulin heavy IGHM Whitney et al. 203932_at major histocompatibility HLA-DMB constant mu complex, class II, Whitney et al. 212998_x_at major histocompatibility HLA-DQB1 DM beta complex, class II, Whitney et al. 204655_at chemokine (C-C motif) CCL5 DQ beta 1 ligand 5 Whitney et al. 212999_x_at major histocompatibility HLA-DQB Whitney et al. 204661_at CDW52 antigen CDW52 complex, class II, (CAMPATH-1 antigen) DQ beta 1 Whitney et al. 205049_s_at CD79A antigen CD79A Whitney et al. 213193_x_at T cell receptor beta locus TRB (immunoglobulin- Whitney et al. 213425_at Homo sapiens cDNA associated alpha) FLJ11441 fis, clone Whitney et al. 205291_at interleukin 2 receptor, IL2RB HEMBA1001323, beta mRNA sequence Whitney et al.
    [Show full text]
  • EMR3 (ADGRE3) Hamster Monoclonal Antibody [Clone ID: 3D7] Product Data
    OriGene Technologies, Inc. 9620 Medical Center Drive, Ste 200 Rockville, MD 20850, US Phone: +1-888-267-4436 [email protected] EU: [email protected] CN: [email protected] Product datasheet for AM01316FC-N EMR3 (ADGRE3) Hamster Monoclonal Antibody [Clone ID: 3D7] Product data: Product Type: Primary Antibodies Clone Name: 3D7 Applications: FC Recommended Dilution: Flow cytometry ( Neat - 1/10): use 10 µl of the suggested working dilution to label 10e6 cells in 100 µl. Reactivity: Human Host: Hamster Isotype: IgG Clonality: Monoclonal Immunogen: ARHO-EMR3-CD97 (EGF1) transfectants. Spleen cells from immunised Armenian hamster were fused with cells of the mouse SP2/0 myeloma cell line. Specificity: This antibody recognises epidermal growth factor (EGF) module-containing mucin-like hormone receptor 3 (EMR3), which is a 56kD member of the EGF-7 transmembrane (TM7) family of adhesion receptors. Formulation: PBS, pH 7.4, containing 0.09% Sodium Azide Label: FITC State: Liquid purified IgG Label: Fluorescein Isothiocyanate Isomer I Concentration: lot specific Purification: Affinity chromatography on Protein G Conjugation: FITC Storage: Store the antibody undiluted at 2-8°C for one month or (in aliquots) at -20°C for longer. Avoid repeated freezing and thawing. This product is photosensitive and should be protected from light. Stability: Shelf life: one year from despatch. Database Link: Entrez Gene 84658 Human Q9BY15 This product is to be used for laboratory only. Not for diagnostic or therapeutic use. View online » ©2021 OriGene Technologies, Inc., 9620 Medical Center Drive, Ste 200, Rockville, MD 20850, US 1 / 2 EMR3 (ADGRE3) Hamster Monoclonal Antibody [Clone ID: 3D7] – AM01316FC-N Background: EMR3 is expressed at the cell surface as a heterodimer.
    [Show full text]
  • Curcumin Alters Gene Expression-Associated DNA Damage, Cell Cycle, Cell Survival and Cell Migration and Invasion in NCI-H460 Human Lung Cancer Cells in Vitro
    ONCOLOGY REPORTS 34: 1853-1874, 2015 Curcumin alters gene expression-associated DNA damage, cell cycle, cell survival and cell migration and invasion in NCI-H460 human lung cancer cells in vitro I-TSANG CHIANG1,2, WEI-SHU WANG3, HSIN-CHUNG LIU4, SU-TSO YANG5, NOU-YING TANG6 and JING-GUNG CHUNG4,7 1Department of Radiation Oncology, National Yang‑Ming University Hospital, Yilan 260; 2Department of Radiological Technology, Central Taiwan University of Science and Technology, Taichung 40601; 3Department of Internal Medicine, National Yang‑Ming University Hospital, Yilan 260; 4Department of Biological Science and Technology, China Medical University, Taichung 404; 5Department of Radiology, China Medical University Hospital, Taichung 404; 6Graduate Institute of Chinese Medicine, China Medical University, Taichung 404; 7Department of Biotechnology, Asia University, Taichung 404, Taiwan, R.O.C. Received March 31, 2015; Accepted June 26, 2015 DOI: 10.3892/or.2015.4159 Abstract. Lung cancer is the most common cause of cancer CARD6, ID1 and ID2 genes, associated with cell survival and mortality and new cases are on the increase worldwide. the BRMS1L, associated with cell migration and invasion. However, the treatment of lung cancer remains unsatisfactory. Additionally, 59 downregulated genes exhibited a >4-fold Curcumin has been shown to induce cell death in many human change, including the DDIT3 gene, associated with DNA cancer cells, including human lung cancer cells. However, the damage; while 97 genes had a >3- to 4-fold change including the effects of curcumin on genetic mechanisms associated with DDIT4 gene, associated with DNA damage; the CCPG1 gene, these actions remain unclear. Curcumin (2 µM) was added associated with cell cycle and 321 genes with a >2- to 3-fold to NCI-H460 human lung cancer cells and the cells were including the GADD45A and CGREF1 genes, associated with incubated for 24 h.
    [Show full text]
  • GPCR Expression in Cancer Cells and Tumors Identifies New
    fphar-09-00431 May 17, 2018 Time: 16:38 # 1 ORIGINAL RESEARCH published: 22 May 2018 doi: 10.3389/fphar.2018.00431 GPCRomics: GPCR Expression in Cancer Cells and Tumors Identifies New, Potential Biomarkers and Therapeutic Targets Paul A. Insel1,2*†, Krishna Sriram1†, Shu Z. Wiley1, Andrea Wilderman1, Trishna Katakia1, Thalia McCann1, Hiroshi Yokouchi1, Lingzhi Zhang1, Ross Corriden1, Dongling Liu1, Michael E. Feigin3, Randall P. French4,5, Andrew M. Lowy4,5 and Fiona Murray1,2,6† 1 Department of Pharmacology, University of California, San Diego, San Diego, CA, United States, 2 Department of Medicine, University of California, San Diego, San Diego, CA, United States, 3 Department of Pharmacology and Therapeutics, Roswell Edited by: Park Comprehensive Cancer Center, Buffalo, NY, United States, 4 Department of Surgery, University of California, San Diego, Ramaswamy Krishnan, San Diego, CA, United States, 5 Moores Cancer Center, University of California, San Diego, San Diego, CA, United States, Harvard Medical School, 6 School of Medicine, Medical Sciences and Nutrition, University of Aberdeen, Aberdeen, United Kingdom United States Reviewed by: G protein-coupled receptors (GPCRs), the largest family of targets for approved drugs, Kevin D. G. Pfleger, Harry Perkins Institute of Medical are rarely targeted for cancer treatment, except for certain endocrine and hormone- Research, Australia responsive tumors. Limited knowledge regarding GPCR expression in cancer cells likely Deepak A. Deshpande, has contributed to this lack of use of GPCR-targeted drugs as cancer therapeutics. Thomas Jefferson University, United States We thus undertook GPCRomic studies to define the expression of endoGPCRs *Correspondence: (which respond to endogenous molecules such as hormones, neurotransmitters and Paul A.
    [Show full text]
  • Multi-Functionality of Proteins Involved in GPCR and G Protein Signaling: Making Sense of Structure–Function Continuum with In
    Cellular and Molecular Life Sciences (2019) 76:4461–4492 https://doi.org/10.1007/s00018-019-03276-1 Cellular andMolecular Life Sciences REVIEW Multi‑functionality of proteins involved in GPCR and G protein signaling: making sense of structure–function continuum with intrinsic disorder‑based proteoforms Alexander V. Fonin1 · April L. Darling2 · Irina M. Kuznetsova1 · Konstantin K. Turoverov1,3 · Vladimir N. Uversky2,4 Received: 5 August 2019 / Revised: 5 August 2019 / Accepted: 12 August 2019 / Published online: 19 August 2019 © Springer Nature Switzerland AG 2019 Abstract GPCR–G protein signaling system recognizes a multitude of extracellular ligands and triggers a variety of intracellular signal- ing cascades in response. In humans, this system includes more than 800 various GPCRs and a large set of heterotrimeric G proteins. Complexity of this system goes far beyond a multitude of pair-wise ligand–GPCR and GPCR–G protein interactions. In fact, one GPCR can recognize more than one extracellular signal and interact with more than one G protein. Furthermore, one ligand can activate more than one GPCR, and multiple GPCRs can couple to the same G protein. This defnes an intricate multifunctionality of this important signaling system. Here, we show that the multifunctionality of GPCR–G protein system represents an illustrative example of the protein structure–function continuum, where structures of the involved proteins represent a complex mosaic of diferently folded regions (foldons, non-foldons, unfoldons, semi-foldons, and inducible foldons). The functionality of resulting highly dynamic conformational ensembles is fne-tuned by various post-translational modifcations and alternative splicing, and such ensembles can undergo dramatic changes at interaction with their specifc partners.
    [Show full text]