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Horse Gene Map a First Generation Radiation Hybrid Map and a Horse-Human-Mouse Comparative Map

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HORSE GENE MAP A FIRST GENERATION RADIATION HYBRID MAP AND A HORSE-HUMAN-MOUSE COMPARATIVE MAP Synteny FISH RH Human Human Draft Mouse map map map homology sequence Chromosome & 0 1CA44 location Draft sequence location 20 1CA30 0 VIASH34 LEX030 ASB41 50 LEX039 LEX020 0 1CA22 18 COMT 22 COMT 16.8 16 17.8 17 1CA44 50 COR079 16 1CA30 COR100 ACTA2 89.5 19 33.8 Synteny FISH RH Human Human Draft Mouse Synteny FISH RH Human Human Draft Mouse Synteny FISH RH Human Human Draft Mouse Synteny FISH RH Human Human Draft Mouse CHA1 ACTA2 15 NV031 RBP4 94.2 19 37.7 map map map homology sequence Chromosome & map map map homology sequence Chromosome & map map map homology sequence Chromosome & map map map homology sequence chromosome & CYPIA2 100 DNTT 96.9 19 40.7 location Draft sequence location Draft sequence location Draft sequence location Draft sequence PAX2 0 PHKB FES 14.3 PAX2 101.3 19 44.6 location location location location 14.2 RBP4/ASB41 IGF1R COR059 14.1 DNTT COL17A1 104.6 19 47.5 0 COR065 INSR COL17A1 0 UCD487 CYP17 103.4 19 46.5 COR041 50 10 20 AHT036 OAT 125.0 7 122.5 ASB18 MYH6 13 LEX020? VHL134 PLAU 40 MYH7 PLAU 74.6 14 15.9 HTG19 CYP17 50 2 ACADL 209.3 1 67.4 SLC30A4 UM002 RBBP4 100 NV029 ANXA7 ANXA7 73.9 14 15.5 0 RBBP4 32.9 4 126.7 12.3 COR059 COR037 0 AHT043 0 TKY041 TKY007 12.2 UCD487 COR090 SLC2A1 4 116.9 PTPN12 IL10 0 ASB12 18 ACADL 1 FUCA1 23.7 133.5* COR028 1CA16 TKY003 4 150 PHKB 37.9 12.1 VHL134 TKY015 SLC2A1 50 MATN1 30.9 128.4 8 - SEMA3C 20 TKY013 17 COR078 4 16 AHT036 GOT2 50 50 1CA20 11 OAT RET 42.8 118.9 FUCA1 HDAC1 32.5 127.0 GOT2 49.1 8 95.6 RET TKY024 4 1CA24 11 MATN1 GOT2 COR033 PTPN12 75.7 5 19.4 AHT024 0 SG25 16 HMGCL 23.6 4 133.5 CES2 57.6 8 104.7 AHT084 12 AHT040 TKY003 HDAC1 15 CES2 200 LEX004 1CA25 CNK 100 GPR3 27.8 4 130.7* SG18 SEMA3C 78.9 5 16.0 ASB12 AHT021 COR078 AHT035 CBFB 57.7 8 105.0 100 100 1CA30 13 FGG 15.3 AT3 UM041 TKY024 GPR3 ELA2A 15.1 4 139.5 14 SG18 1CA32 SG02/SG25 50 PACE CBFB 16 KCC1 58.6 8 105.7 AHT048 TCRG TCRG 37.8 13 18.7 HFABP-L AHT035 HMS54 ALPL 21.4 4 135.3 250 16 TKY041 IL10 205.6 1 131.8 14 AHT021/1CA20 FES 15.1 HMGCL 150 KCC1 18 1CA43 ASB17 RHD 25.2 4 132.4 ADD1 AHT022 150 HMS06 LAMC1 MEF2A/FES 0 1CA32 MEF2A 96.8 7 56.6 NPPA GPR3 GLG1 65.4 8 111.0 15 TCRG GCK 43.8 11 71.1 17 LAMC2 150 LAMC2 180.6 1 154.0 ASB08 15 ASB08 D29580 28.7 13 AHT022 PACE FES 87.6 7 69.8* 14 ASB17 UM007 ADH2 GLG1 KARS 66.5 8 111.9 COL1A214 PRG4 AT3 171.4 1 162.1 COR006 AHT040/1CA41 LEX077 ELA2A/ALPL ECE1 21.1 300 GLG1 GCK GCK 16 AHT024 16 PACE 87.6 7 69.8* 200 HMS51 4 135.5* ADH3 KARS CSF2 PTGS2 LAMC1 180.5 1 154.1 1CA41 RHD/NPPA ALPL DPEP1 81.0 8 123.2 13 200 COR046 50 13 HP1-BP74 20.6 4 135.8 12 DPEP1 KARS VHL66 COR046 1CA24 7 D29580 ECE1 ALB MC1R 81.3 8 123.4 PTGS2 PRG4 183.7 1 151.3 COR053 IGF1R 95.8 57.4 12 MC1R EN2 ASB03 17.1 LEX058 COR046 A-14 HP1-BP74 EIF4G3 20.7 4 135.6* 11 UMNe063 AT3 15 PTGS2 184.1 1 150.9 11 PGD CCNI 350 LEX057 12 LAMB3 0 PKLR COR059 TJP1 TJP1 25.4 7 54.7 250 11 LEP GBA LAMB3 208.4 1 194.8 100 1CA20 15 ASB13 11 EIF4G3 NPPA 11.9* 4 143.3* MC1R 11 250 HMS76 GBA COR063 17.2 FGFR3 SG33 1CA43 UCD380 PGD 10.4 4 144.5* 12 MEST ASB03 LAMC1 PKLR 153.1 3 89.9 LEX058 ASB17 12 KARS HMS61 11 HGF 79.8 5 14.9 COR079 UMNe54 14 50 CTSK GBA 153.0 3 90.0 17.3 1CA25 IGF1R COR026 300 400 TCRG HGF 0 NGFB COR100 MC1R 13 12 COR089 COL1A2 92.5 6 4.2 CTSK 148.6 3 95.7 150 13 MTP ADH2 100.4 3 138.9 VDUP1 1CA28 COR035 NPPA AHT090 VCAM1 13 VDUP1 143.9 3 96.8 TKY002 SPARCL1 PDHA2 ADH3 100.5 3 138.7 ASB22 VDUP1 GJA5 1 21.1 TJP1 COR037 13 LAMB1 GJA5 145.4 3 97.3 HMS07 COR051 UCD437 PDHA2 96.9 3 141.7 COR047 LEX033 106.0 S100A6 PK3 50 LAMB1 12 25.3 12 0 CD2 200 TKY002 COR041 4 MTP 100.7 3 138.5 14.1 S100A6 146.47 3 91.4 HTG12 21.2 9 58.2 14.1 0 ADH2/ADH3 HTG07 L16464 NGFB 1CA43 CYP1A2 70.9 0 COR049 LOC51170 88.4 5 101.6* COR089 11 L16464 154.9 LEX20 1CA25 COR043 14.2 14 CD2 COR023 CD2 117.8 3 101.3 21.3 PKM2 PK3 68.2 9 60.2 14.2 A-14(ms) CLU 27.2 57.0 AHT013 11 LEX30 0 TKY106 COR049 8 14 COR005 HNRPDL 83.2 5 97.5 HMS06 100 68.2 9 60.2* LEX050 12 NFIA 50 UCD304 NFIA 61.4 4 95.5 UCD493 PKM2 CLU 14.3 ALB 50 LOC51170 ASB22 LEX58LEX39 COR051 14.3 50 COR028 HMS09 7 HMS05 ATP1A1 117.4 3 101.6 22 UM004 CYP1A2 ANXA2 56.1 9 70.0 4 CCNI 77.8 5 92.8 LEX061 ATP1A1 LEX77 COR078 21.1 13 NGFB ANXA2 50 UM043 MYO5A 48.1 9 75.7 COR033 HNRPDL HMS19 150 116.2 3 102.5 SG25 AHT012 ALB 73.9 5 90.0 COR023 100 MYO5A PK3 COR090 ASB13 PDGFRA VCAM1 SORD 40.6 2 123.2* 21 100 HMS22 HMS19 ASB29 HTG15 VCAM1 101.9 3 116.4 UCD440 23 GRP58 PKM2 21.1 100 LEX07 F11 ? CCNI PDGFRA 54.8 5 74.4 21.2 HMS05 IGL@ GRP58 39.4 2 122.3 COR094 KIT HMB6 14 IGL@ 19.2 16 18.5 UCD487 THBS1 HTG12 A-14 LEX57 HTG07 HTG15 TSHB 24 100 THBS1 35.2 2 119.0 TKY003 KIT 55.3 5 74.8 HTG09 200 VCAM1 UCD493 SORD 2 114.9 21.2 ASB13 22.1 21.3 COL1A2 150 AHT058 ACTC 30.4 FGG 150 4 FGG 156.3 3 83.7 150 HTG09 LEX04 TSHB 115.9 3 102.8 COR006 UCD380 SG18 22.2 CSN1,2 ALB CFTR 115.5 6 18.1 UM002 25 UM004 21.3 SMARCA5 FGG KIT 70.7 5 87.2 0 HMS19 15 NRAS NRAS 115.6 3 103.1 1 FABP3 31.6 0 CSN1,2 LEX33 LEX14 UM004 HMS7 150 ANXA2 UM007 4 127.8 UCD437 22.3 ASB23 22 CFTR SH3GLB1 87.7 3 45.2 FABP3 ASB23 HTG09 LEX34 200 26 UCD440 UCHL1 UCHL1 41.3 5 65.7 LEX50 UOX ASB10 UM043 MYH6 CMA1 22.3 14 47.0 200 HTG02 TGM1 MY05A 22 SMARCA5 145.2 8 80.3* 23 CFTR LEP 126.3 6 29.0 UCD304 16 SH3GLB1 VHL134 27 COR006 MYH6 21.2 14 46.0 4 23 50 48.1 5 71.8 LEX61 AKR1B1 UOX 3 147.1 ACTC 0 UCHL1 TXK LEP MEST 128.6 6 30.7* LEX014 HMS07 14 TGM1 22.0 14 46.7 23 IL2 124.2 3 37.0 24 0 250 VIAS-H34 28 NP IL2 COR094 24 TXK HMS09 LEX034 NP 18.3 12 42.8 24 LEX007 3 CCK 41.5 9 122.9 SG23 AKR1B1 132.4 6 34.4 CMA1 25 CCK 26 DIA1 22 DIA1 39.6 15 83.9 MGAT2 0 UMNe 76 ADD1 2.8 5 33.2 CLCN1 MEST 17 29 MYH6 MGAT2 47.4 12 63.8* 25 26 100 OPN1SW 126.8 6 29.3 50 ADD1 27 OPN1SW COR047 20 COR005 0 300 NP EN2 CLCN1 141.3 6 42.4* LEX014 SMARCA5 AHT097 SG23 HMS62 1CA16 EN2 153.4 5 26.6 1 0 COR053 2 COR035 3 4 CLCN1 5 0 50 20 1CA40 COR026 HTG22 COR063 20 COR043 AHT061 0 AHT042 HTG31 EN2 0 AHT005 0 RYR1 0 COR019 SG23 COR045 FN1 FN1 214.4 1 72.2 COR097 AHT096 6.7 17 56.2 0 15 FN1 MAP2 208.7 1 66.9 C3 50 COR020 50 MAP2 APOA4 C3 19 50 HMS03 CHRNG 16 LDLR 11.3 9 21.8 UBE2L3 INHA INHA 218.4 1 76.3 C3 LDLR 14 PAX3 TKY34 PGR 103.1 9 8.8 2 PGR UBE2L3 18.6 16 16.6 SLC7A10 UCD482 FN1 DRD2 TKY35 50 VHL126 CUL3 PAX3 221.1 1 78.9 15 MMP13 0 DRD2 MMP13 105.0 9 7.2 100 BCR 20.2 10 75.4* RYR1 100 13 100 HBB APOA4 TKY12 AHT025 22 GPI GAPD SCG2 COR010 APOA4 119.0 9 46.4 BCR LIF 27.3 11 4.1 COR008 COR048 SCG2 222.4 1 80.3 PTH TKY034/035 LEX015 17 AHT025 16 TKY023? XRCC1 IFNG NV082 THY1 112.5 LIMK2 28.3 1 3.2 COR013 CUL3 223.3 1 81.1 THY1 TKY012 FDX1 9 52.2 TCF1 100 COR045 12 14.3 APOC3 16 CCND2 150 15 150 SLC7A10 34.3 7 25.6 UGT1A1 150 FDX1 LEX038 DRD2 115.6 9 49.6 LIMK2 HTG08 UCD482 AHT015 MAP2 UGT1A1 232.6 1 88.6 TUB 14.2 LDHA SART3 CCND2 4.1 6 128.0 ARPC3 15 COR048 GPI 35.4 7 24.6 TYR TKY283 LDHA 19.5 7 36.4 15 LIF 14 AMD1 0 ASB06 11 231.4 1 87.6 APOC3 0 11 UMNe70 TCF1 120.2 5 112.9 DNAPK 14 AHT015 RYR1 39.5 7 21.2 PAX3 LEX065 CHRNG 14.1 150 NV018 TKY005 THY1 121.2 9 44.3 NOS1 0 UCD046 ARG1 ASB06 XRCC1 44.6 7 16.7 11 200 APOA1 NOS1 116.6 5 115.8 TG CHRNG HTG33 119.0 9 TCF1 14 SART3 12 LEX070 LHB/CKM CKM 19 PFKM 13 0 APOC3 46.4 UM034 SART3 108.0 5 111.6 13 CRH 66.2 3 19.4* CGA 13 SG30 CKM 46.4 7 14.4 12 TKY272 APOA1 119.0 9 46.4 CRH NKX3A 50 VWF 5.9 6 126.4 TYMS 13 HPD TKY006? 0 COR015 SG30 LHB 50.1 7 34.9 SILV HPD 121.1 5 121.2 PRKDC 47.8 16 15.1* CKM SG20 0 HMS55 12 TKY005 COR004 12 LEX023 50 12 PRKDC SFTPC ERCC2 46.4 7 14.3 TPI1 FLJ11021 121.6 5 121.8* COL10A 12 UM028 COR015 13 VWF 11 50 LEX045 11 FLJ11021 11 SFTPC LPL NKX3A 23.2 14 60.3 COR083 NR1H2 PEX7 100 LEX008 UM015 11 COR095 11 ASB38 10.0 11 0 COR098 11 UCD412 AHT05 VAPA 17 64.6 SFTPC 21.7 14 61.4 LEX062 50 COR004 12 TYR 12 TYMS 100 COR008 12 SG20 19 NR1H2 51.5 7 34.1 LPL 19.6 8 68.2 AHT086 11 LEX066 21.1 100 ASB14 LEX023 13 LPL COR095 TKY282 TYR 91.2 7 77.1 13 NPC1 TYMS 0.9 5 28.5 COR013 12 ERCC2 UM028 COR010 13 50 8 DEFB1 6.7 8 20.5 ASB06 150 COX8 COR003 DEFB1 COR093 ME1 COR083 100 LEX015 COX8 66.1 19 LAMA3 150 LEX029 NPC1 21.0 18 12.2 COR093 14 PLAT 41.4 8 21.4 ASB09 13 21.2 TKY111 99.0 SG28 COR012 PLAT COR019 12 PFKM 48.5 15 WT1 34.0 2 106.0 14 CDH2 COR015 UCD412 150 COR098 UM037 ANK1 41.9 21.7 14 LEX045 14 UMNe74 COR056 DSG2 0 VAPA LAMA3 21.3 18 12.3 8 200 COR070 OPCML 134.4 9 28.5* 100 COR020 21.3 15 HMS03 LEX062/066 150 NV081 HBB HBB 11 5.9 7 93.4 COR097 ASB14 15 ANK1 HSPC038 COR045 15 SG28 15 HBB CDH2 25.4 18 16.6 HSPC038 101.2 15 0 CASP8AP2 CASP8AP2 90.4 4 32.2 HTG31 HBE1 200 16 HTG08 UCD465 TRA1 103.4 10 86.8 TUB HBE1 6.0 7 93.6 LEX23 TYMS DSC2 29.1 18 20.1 OAZIN 102.8 38.6 COR048 16 CGA 87.7 RKJ06 POU2F2 50 15 COL10A1 6 CGA 4 34.5 POU2F2 43.2 7 17.3 LEX19 150 OAZIN COR083 LEX65 22 TRA1 COR070 IFNG 68.0 10 118.5 16 OPCML LYVE-1 19 LEX29 SG32 18 DSG2 29.1 18 20.1 NOV 119.4 15 55.1 17 SG17 ME1 ME1 83.8 9 87.5 200 TUB 8.8 7 98.5 LAMA3 COR085 AMD1 PKFM LYVE-1 21.1 LEX70 MYC 127.7 15 62.4 NV007 AMD1 111.0 10 40.3 UCD465 MAN1 64.9 10 121.2 17 250 PTH 11.5 7 SG32 16 21 ASB09 IFNG INSL3 LYVE-1 100.4 100 COR012 TG 132.6 15 67.1 HMS02 0 COL10A1 WIF1 64.9 10 UCD046 21.2 GALR1 74.5 18 82.9 UM037 MYC 200 UM015 23 SILV RKJ06 121.2 CNTF PTH 14.7 7 102.9 AHT053 LEX08 UM040 COL10A1 116.2 10 34.3 250 18 PAX6 21.3 17 ASB05 SG17 SILV 56.2 10 129.3 19 INSL3 18.4 8 UM033 CDH2 VHL126 LEX09 300 22 HSPC039 44.9 18 77.3* NOV 12 ARPC3 109.8 5 120.4 22 PEX7 24 BDNF CNTF 60.7 19 12.2 UM070 150 18 LEX62 50 AMD1 ARG1 131.5 10 19 AHT019 23 PAI2 DSC2 250 CGA? 24.8 11 PAX6 33.4 2 106.5 NARS 55.6 18 64.8*
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    SAGE-Hindawi Access to Research International Journal of Alzheimer’s Disease Volume 2010, Article ID 604792, 56 pages doi:10.4061/2010/604792 Research Article Complex and Multidimensional Lipid Raft Alterations in a Murine Model of Alzheimer’s Disease Wayne Chadwick, 1 Randall Brenneman,1, 2 Bronwen Martin,3 and Stuart Maudsley1 1 Receptor Pharmacology Unit, National Institute on Aging, National Institutes of Health, 251 Bayview Boulevard, Suite 100, Baltimore, MD 21224, USA 2 Miller School of Medicine, University of Miami, Miami, FL 33124, USA 3 Metabolism Unit, National Institute on Aging, National Institutes of Health, 251 Bayview Boulevard, Suite 100, Baltimore, MD 21224, USA Correspondence should be addressed to Stuart Maudsley, [email protected] Received 17 May 2010; Accepted 27 July 2010 Academic Editor: Gemma Casadesus Copyright © 2010 Wayne Chadwick et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Various animal models of Alzheimer’s disease (AD) have been created to assist our appreciation of AD pathophysiology, as well as aid development of novel therapeutic strategies. Despite the discovery of mutated proteins that predict the development of AD, there are likely to be many other proteins also involved in this disorder. Complex physiological processes are mediated by coherent interactions of clusters of functionally related proteins. Synaptic dysfunction is one of the hallmarks of AD. Synaptic proteins are organized into multiprotein complexes in high-density membrane structures, known as lipid rafts. These microdomains enable coherent clustering of synergistic signaling proteins.
  • Novel Insights Into the Pathophysiology of Peripherin-2 Mutations in Rod and Cone Photoreceptors

    Novel Insights Into the Pathophysiology of Peripherin-2 Mutations in Rod and Cone Photoreceptors

    Dissertation zur Erlangung des Doktorgrades der Fakultät für Chemie und Pharmazie der Ludwig-Maximilians-Universität München Novel Insights into the Pathophysiology of Peripherin-2 Mutations in Rod and Cone Photoreceptors Sybille Böhm aus Schäßburg, Rumänien 2018 Erklärung Diese Dissertation wurde im Sinne von § 7 der Promotionsordnung vom 28. November 2011 von Herrn Prof. Dr. Martin Biel betreut. Eidesstattliche Versicherung Diese Dissertation wurde eigenständig und ohne unerlaubte Hilfe erarbeitet. München, den 12.10.2018 _______________________ (Sybille Böhm) Dissertation eingereicht am 12.10.2018 1. Gutachter: Prof. Dr. Martin Biel 2. Gutachter: PD Dr. Stylianos Michalakis Mündliche Prüfung am 18.12.2018 Table of contents 3 Table of contents 1 Preface .........................................................................................................................7 2 Introduction .................................................................................................................8 2.1 Anatomy of the retina .................................................................................................... 8 2.2 Anatomy of photoreceptors .......................................................................................... 9 2.3 Inherited retinal diseases ............................................................................................ 10 2.3.1 Retinitis pigmentosa ....................................................................................................... 10 2.4 Peripherin-2 .................................................................................................................
  • CD82 Protects Against Glaucomatous Axonal Transport De Cits Via Mtorc1 Activation in Mice

    CD82 Protects Against Glaucomatous Axonal Transport De Cits Via Mtorc1 Activation in Mice

    CD82 Protects Against Glaucomatous Axonal Transport Decits via mTORC1 Activation in Mice Yin Zhao Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology https://orcid.org/0000-0002-1470-7184 Meng Ye Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology Jingqiu Huang Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology Qianxue Mou Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology Jing Luo Huazhong University of Science and Technology Yuanyuan Hu Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology Xiaotong Lou Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology Ke Yao Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology Bowen Zhao Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology Qiming Duan Gladstone Institute of Cardiovascular Disease Xing Li Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology Hong Zhang ( [email protected] ) Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology Research article Keywords: Glaucoma, progressive optic nerve degeneration, retinal ganglion cell, optic nerve Posted Date: April 14th, 2021 DOI: https://doi.org/10.21203/rs.3.rs-404388/v1 Page 1/35 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Page 2/35 Abstract Background: Glaucoma is a leading cause of irreversible blindness worldwide characterized by progressive optic nerve degeneration and retinal ganglion cell (RGC) loss.
  • Mouse Models of Inherited Retinal Degeneration with Photoreceptor Cell Loss

    Mouse Models of Inherited Retinal Degeneration with Photoreceptor Cell Loss

    cells Review Mouse Models of Inherited Retinal Degeneration with Photoreceptor Cell Loss 1, 1, 1 1,2,3 1 Gayle B. Collin y, Navdeep Gogna y, Bo Chang , Nattaya Damkham , Jai Pinkney , Lillian F. Hyde 1, Lisa Stone 1 , Jürgen K. Naggert 1 , Patsy M. Nishina 1,* and Mark P. Krebs 1,* 1 The Jackson Laboratory, Bar Harbor, Maine, ME 04609, USA; [email protected] (G.B.C.); [email protected] (N.G.); [email protected] (B.C.); [email protected] (N.D.); [email protected] (J.P.); [email protected] (L.F.H.); [email protected] (L.S.); [email protected] (J.K.N.) 2 Department of Immunology, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700, Thailand 3 Siriraj Center of Excellence for Stem Cell Research, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700, Thailand * Correspondence: [email protected] (P.M.N.); [email protected] (M.P.K.); Tel.: +1-207-2886-383 (P.M.N.); +1-207-2886-000 (M.P.K.) These authors contributed equally to this work. y Received: 29 February 2020; Accepted: 7 April 2020; Published: 10 April 2020 Abstract: Inherited retinal degeneration (RD) leads to the impairment or loss of vision in millions of individuals worldwide, most frequently due to the loss of photoreceptor (PR) cells. Animal models, particularly the laboratory mouse, have been used to understand the pathogenic mechanisms that underlie PR cell loss and to explore therapies that may prevent, delay, or reverse RD. Here, we reviewed entries in the Mouse Genome Informatics and PubMed databases to compile a comprehensive list of monogenic mouse models in which PR cell loss is demonstrated.
  • Antibodieseses F F Orforor Neuroscience Neurneoscieuroscienncece

    Antibodieseses F F Orforor Neuroscience Neurneoscieuroscienncece

    antibodiantibodiantibodieseses f f orforor neuroscience neurneoscieuroscienncece ptglab.coptglab.comm antibodies people trust ptglab.com antibodies people trust ptglab.com antibodies people trust Antibodies for Neuroscience 3 PROTEINTECH: SETTING THE BENCHMARK IN ANTIBODIES ORIGINAL MANUFACTURER Part of Proteintech’s early vision was to make all its own products, to the highest standards possible, thus assuming ultimate responsibility for their quality. In addition ORIGINAL PRODUCTS to its founders’ refusal to source a single antibody from any other provider, they also refused to supply any other provider. When you receive your antibody and see the Proteintech logo on the vial, know that you hold something that is truly unique. As an original manufacturer, Proteintech can offer you: • 100% original products; each product is unique and can only be bought directly or through approved distributors. • Antibodies now tested in siRNA–treated samples to demonstrate antibody specificity. • Guaranteed to work in any species and any applications, or get your money back. siRNA Recently, Proteintech has pledged to undertake siRNA knockdown validation of most of its antibodies by the end of 2015. The specificities of over 550 of its antibodies VALIDATION have already been confirmed by customers using siRNA knockdown, and published in over 650 journal papers. In adding its own siRNA data to those previously available in the literature, Proteintech’s aim is to make a gold standard of antibody validation more accessible to its customers. • Help set a