Cat# Item Applications Reactivity BT-AP00001 11Β-HSD1 Polyclonal

Total Page：16

File Type：pdf, Size：1020Kb

Cat# Item Applications Reactivity BT-AP00001 11β-HSD1 Polyclonal Antibody WB,IHC-p,ELISA Human,Mouse,Rat BT-AP00002 11β-HSD1 Polyclonal Antibody WB,IHC-p,ELISA Human,Mouse,Rat BT-AP00003 14-3-3 β Polyclonal Antibody WB,IHC-p,IF,ELISA Human,Mouse,Rat BT-AP00004 14-3-3 β/ζ Polyclonal Antibody WB,IHC-p,ELISA Human,Mouse,Rat BT-AP00005 14-3-3 γ Polyclonal Antibody WB,IHC-p,IF,ELISA Human,Mouse,Rat BT-AP00006 14-3-3 ε Polyclonal Antibody WB,IHC-p,IF,ELISA Human,Mouse,Rat BT-AP00007 14-3-3 ε Polyclonal Antibody WB,IHC-p Mouse,Rat BT-AP00008 14-3-3 ζ Polyclonal Antibody WB,IHC-p,ELISA Human,Mouse,Rat BT-AP00009 14-3-3 ζ Polyclonal Antibody WB,IHC-p,IP,IF,ELISA Human,Mouse,Rat BT-AP00010 14-3-3 ζ/δ Polyclonal Antibody WB,IHC-p,IF,ELISA Human,Mouse,Rat BT-AP00011 14-3-3 η Polyclonal Antibody WB,IHC-p,IF,ELISA Human,Mouse,Rat BT-AP00012 14-3-3 θ Polyclonal Antibody WB,IHC-p,IF,ELISA Human,Mouse,Rat BT-AP00013 14-3-3 θ/τ Polyclonal Antibody WB,IHC-p,IF,ELISA Human,Mouse,Rat BT-AP00014 14-3-3 σ Polyclonal Antibody WB,IHC-p,ELISA Human,Mouse 14-3-3-pan (Acetyl Lys51/49) BT-AP00015 Polyclonal Antibody WB,ELISA Human,Mouse,Rat BT-AP00016 17β-HSD11 Polyclonal Antibody WB,ELISA Human BT-AP00017 17β-HSD4 Polyclonal Antibody WB,IHC-p,ELISA Human,Mouse,Rat BT-AP00018 2A5B Polyclonal Antibody WB,ELISA Human BT-AP00019 2A5E Polyclonal Antibody WB,ELISA Human,Mouse BT-AP00020 2A5G Polyclonal Antibody WB,ELISA Human,Mouse BT-AP00021 2AAA Polyclonal Antibody WB,ELISA Human,Mouse BT-AP00022 2ABG Polyclonal Antibody WB,ELISA Human,Rat,Mouse BT-AP00023 2B1F Polyclonal Antibody WB,ELISA Human BT-AP00024 3BHS1 Polyclonal Antibody WB,ELISA Human BT-AP00025 3BHS2 Polyclonal Antibody WB,ELISA Human BT-AP00026 3BP1 Polyclonal Antibody WB,ELISA Human,Mouse BT-AP00027 3BP2 Polyclonal Antibody WB,ELISA Human BT-AP00028 3HAO Polyclonal Antibody WB,ELISA Human,Mouse,Rat BT-AP00029 3MG Polyclonal Antibody WB,ELISA Human BT-AP00030 3pK Polyclonal Antibody WB,IHC-p,IF,ELISA Human,Mouse,Rat BT-AP00031 3β-HSD7 Polyclonal Antibody WB,ELISA Human,Mouse,Rat BT-AP00032 4.1G Polyclonal Antibody WB,IHC-p,ELISA Human BT-AP00033 4.

477

Copy Link

Recommended publications

Supplementary Data
Supplementary Data for Quantitative Changes in the Mitochondrial Proteome from Subjects with Mild Cognitive Impairment, Early Stage and Late Stage Alzheimer’s disease Table 1 - 112 unique, non-redundant proteins identified and quantified in at least two of the three analytical replicates for all three disease stages. Table 2 - MCI mitochondrial samples, Protein Summary Table 3 - MCI mitochondrial samples, Experiment 1 Table 4 - MCI mitochondrial samples, Experiment 2 Table 5 - MCI mitochondrial samples, Experiment 3 Table 6 - EAD Mitochondrial Study, Protein Summary Table 7 - EAD Mitochondrial Study, Experiment 1 Table 8 - EAD Mitochondrial Study, Experiment 2 Table 9 - EAD Mitochondrial Study, Experiment 3 Table 10 - LAD Mitochondrial Study, Protein Summary Table 11 - LAD Mitochondrial Study, Experiment 1 Table 12 - LAD Mitochondrial Study, Experiment 2 Table 13 - LAD Mitochondrial Study, Experiment 3 Supplemental Table 1. 112 unique, non-redundant proteins identified and quantified in at least two of the three analytical replicates for all three disease stages. Description Data MCI EAD LAD AATM_HUMAN (P00505) Aspartate aminotransferase, mitochondrial precursor (EC Mean 1.43 1.70 1.31 2.6.1.1) (Transaminase A) (Glutamate oxaloacetate transaminase 2) [MASS=47475] SEM 0.07 0.09 0.09 Count 3.00 3.00 3.00 ACON_HUMAN (Q99798) Aconitate hydratase, mitochondrial precursor (EC 4.2.1.3) Mean 1.24 1.61 1.19 (Citrate hydro-lyase) (Aconitase) [MASS=85425] SEM 0.05 0.17 0.18 Count 3.00 2.00 3.00 ACPM_HUMAN (O14561) Acyl carrier protein, mitochondrial
[Show full text]
Endothelin System and Therapeutic Application of Endothelin Receptor
xperim ACCESS Freely available online & E en OPEN l ta a l ic P in h l a C r m f o a c l a o n l o r g u y o J Journal of ISSN: 2161-1459 Clinical & Experimental Pharmacology Research Article Endothelin System and Therapeutic Application of Endothelin Receptor Antagonists Abebe Basazn Mekuria, Zemene Demelash Kifle*, Mohammedbrhan Abdelwuhab Department of Pharmacology, School of Pharmacy, College of Medicine and Health Sciences, University of Gondar, Gondar, Ethiopia ABSTRACT Endothelin is a 21 amino acid molecule endogenous potent vasoconstrictor peptide. Endothelin is synthesized in vascular endothelial and smooth muscle cells, as well as in neural, renal, pulmonic, and inflammatory cells. It acts through a seven transmembrane endothelin receptor A (ETA) and endothelin receptor B (ETB) receptors belongs to G protein-coupled rhodopsin-type receptor superfamily. This peptide involved in pathogenesis of cardiovascular disorder like (heart failure, arterial hypertension, myocardial infraction and atherosclerosis), renal failure, pulmonary arterial hypertension and it also involved in pathogenesis of cancer. Potentially endothelin receptor antagonist helps the treatment of the above disorder. Currently, there are a lot of trails both per-clinical and clinical on endothelin antagonist for various cardiovascular, pulmonary and cancer disorder. Some are approved by FAD for the treatment. These agents are including both selective and non-selective endothelin receptor antagonist (ETA/B). Currently, Bosentan, Ambrisentan, and Macitentan approved
[Show full text]
Gene Symbol Gene Description ACVR1B Activin a Receptor, Type IB
Table S1. Kinase clones included in human kinase cDNA library for yeast two-hybrid screening Gene Symbol Gene Description ACVR1B activin A receptor, type IB ADCK2 aarF domain containing kinase 2 ADCK4 aarF domain containing kinase 4 AGK multiple substrate lipid kinase;MULK AK1 adenylate kinase 1 AK3 adenylate kinase 3 like 1 AK3L1 adenylate kinase 3 ALDH18A1 aldehyde dehydrogenase 18 family, member A1;ALDH18A1 ALK anaplastic lymphoma kinase (Ki-1) ALPK1 alpha-kinase 1 ALPK2 alpha-kinase 2 AMHR2 anti-Mullerian hormone receptor, type II ARAF v-raf murine sarcoma 3611 viral oncogene homolog 1 ARSG arylsulfatase G;ARSG AURKB aurora kinase B AURKC aurora kinase C BCKDK branched chain alpha-ketoacid dehydrogenase kinase BMPR1A bone morphogenetic protein receptor, type IA BMPR2 bone morphogenetic protein receptor, type II (serine/threonine kinase) BRAF v-raf murine sarcoma viral oncogene homolog B1 BRD3 bromodomain containing 3 BRD4 bromodomain containing 4 BTK Bruton agammaglobulinemia tyrosine kinase BUB1 BUB1 budding uninhibited by benzimidazoles 1 homolog (yeast) BUB1B BUB1 budding uninhibited by benzimidazoles 1 homolog beta (yeast) C9orf98 chromosome 9 open reading frame 98;C9orf98 CABC1 chaperone, ABC1 activity of bc1 complex like (S. pombe) CALM1 calmodulin 1 (phosphorylase kinase, delta) CALM2 calmodulin 2 (phosphorylase kinase, delta) CALM3 calmodulin 3 (phosphorylase kinase, delta) CAMK1 calcium/calmodulin-dependent protein kinase I CAMK2A calcium/calmodulin-dependent protein kinase (CaM kinase) II alpha CAMK2B calcium/calmodulin-dependent
[Show full text]
Novel Binding Partners of PBF in Thyroid Tumourigenesis
NOVEL BINDING PARTNERS OF PBF IN THYROID TUMOURIGENESIS By Neil Sharma A thesis presented to the College of Medical and Dental Sciences at the University of Birmingham for the Degree of Doctor of Philosophy Centre for Endocrinology, Diabetes and Metabolism, School of Clinical and Experimental Medicine August 2013 University of Birmingham Research Archive e-theses repository This unpublished thesis/dissertation is copyright of the author and/or third parties. The intellectual property rights of the author or third parties in respect of this work are as defined by The Copyright Designs and Patents Act 1988 or as modified by any successor legislation. Any use made of information contained in this thesis/dissertation must be in accordance with that legislation and must be properly acknowledged. Further distribution or reproduction in any format is prohibited without the permission of the copyright holder. SUMMARY Thyroid cancer is the most common endocrine cancer, with a rising incidence. The proto-oncogene PBF is over-expressed in thyroid tumours, and the degree of over-expression is directly linked to patient survival. PBF causes transformation in vitro and tumourigenesis in vivo, with PBF-transgenic mice developing large, macro-follicular goitres, effects partly mediated by the internalisation and repression of the membrane-bound transporters NIS and MCT8. NIS repression leads to a reduction in iodide uptake, which may negatively affect the efficacy of radioiodine treatment, and therefore prognosis. Work within this thesis describes the use of tandem mass spectrometry to produce a list of potential binding partners of PBF. This will aid further research into the pathophysiology of PBF, not just in relation to thyroid cancer but also other malignancies.
[Show full text]
Impaired Cellular Immunity in the Murine Neural Crest Conditional Deletion of Endothelin Receptor-B Model of Hirschsprung’S Disease
RESEARCH ARTICLE Impaired Cellular Immunity in the Murine Neural Crest Conditional Deletion of Endothelin Receptor-B Model of Hirschsprung’s Disease Ankush Gosain1,2*, Amanda J. Barlow-Anacker1, Chris S. Erickson1, Joseph F. Pierre1, Aaron F. Heneghan1, Miles L. Epstein2, Kenneth A. Kudsk1,3 a11111 1 Department of Surgery, University of Wisconsin-Madison School of Medicine and Public Health, Madison, Wisconsin, United States of America, 2 Department of Neuroscience, University of Wisconsin-Madison School of Medicine and Public Health, Madison, Wisconsin, United States of America, 3 Veteran Administration Surgical Service, William S. Middleton Memorial Veterans Hospital, Madison, United States of America * [email protected] OPEN ACCESS Citation: Gosain A, Barlow-Anacker AJ, Erickson Abstract CS, Pierre JF, Heneghan AF, Epstein ML, et al. (2015) Impaired Cellular Immunity in the Murine Hirschsprung’s disease (HSCR) is characterized by aganglionosis from failure of neural crest Neural Crest Conditional Deletion of Endothelin cell (NCC) migration to the distal hindgut. Up to 40% of HSCR patients suffer Hirschsprung’s- Receptor-B ’ Model of Hirschsprung s Disease. PLoS associated enterocolitis (HAEC), with an incidence that is unchanged from the pre-operative ONE 10(6): e0128822. doi:10.1371/journal. pone.0128822 to the post-operative state. Recent reports indicate that signaling pathways involved in NCC migration may also be involved in the development of secondary lymphoid organs. We hy- Academic Editor: Anatoly V. Grishin, Childrens Hospital Los Angeles, UNITED STATES pothesize that gastrointestinal (GI) mucosal immune defects occur in HSCR that may contrib- ute to enterocolitis. EdnrB was deleted from the neural crest (EdnrBNCC-/-) resulting in mutants Received: November 12, 2014 with defective NCC migration, distal colonic aganglionosis and the development of enterocoli- Accepted: May 1, 2015 tis.
[Show full text]
Fasciola Hepatica
Fasciola hepatica Robinson, M., Dalton, J., O'Brien, B., & Donnelly, S. (2013). Fasciola hepatica: The therapeutic potential of a worm secretome. International Journal for Parasitology, 43(3-4), 283–291. https://doi.org/10.1016/j.ijpara.2012.11.004 Published in: International Journal for Parasitology Document Version: Peer reviewed version Queen's University Belfast - Research Portal: Link to publication record in Queen's University Belfast Research Portal Publisher rights NOTICE: this is the author’s version of a work that was accepted for publication in International Journal for Parasitology. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in International Journal for Parasitology, [VOL 43, ISSUE 2-3, 2013] General rights Copyright for the publications made accessible via the Queen's University Belfast Research Portal 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 Research Portal is Queen's institutional repository that provides access to Queen's research output. Every effort has been made to ensure that content in the Research Portal does not infringe any person's rights, or applicable UK laws. If you discover content in the Research Portal that you believe breaches copyright or violates any law, please contact [email protected].
[Show full text]
Proteomics and Phylogenetic Analysis of the Cathepsin L
Research Proteomics and Phylogenetic Analysis of the Cathepsin L Protease Family of the Helminth Pathogen Fasciola hepatica EXPANSION OF A REPERTOIRE OF VIRULENCE-ASSOCIATED FACTORS* Mark W. Robinson‡§¶, Jose F. Tort‡ʈ, Jonathan Lowther‡, Sheila M. Donnelly‡, Emily Wong‡, Weibo Xu‡, Colin M. Stack‡**, Matthew Padula‡‡, Ben Herbert‡‡, and John P. Dalton‡§§ Cathepsin L proteases secreted by the helminth pathogen zymes. The prosegment region was highly conserved Fasciola hepatica have functions in parasite virulence in- between the clades except at the boundary of prosegment cluding tissue invasion and suppression of host immune and mature enzyme. Despite the lack of conservation at this Downloaded from responses. Using proteomics methods alongside phylo- section, sites for exogenous cleavage by asparaginyl en- genetic studies we characterized the profile of cathepsin dopeptidases and a Leu-Ser2His motif for autocatalytic L proteases secreted by adult F. hepatica and hence iden- cleavage by cathepsin Ls were preserved. Molecular & tified those involved in host-pathogen interaction. Phylo- Cellular Proteomics 7:1111–1123, 2008. genetic analyses showed that the Fasciola cathepsin L gene family expanded by a series of gene duplications https://www.mcponline.org followed by divergence that gave rise to three clades associated with mature adult worms (Clades 1, 2, and 5) The helminth pathogens Fasciola hepatica and Fasciola and two clades specific to infective juvenile stages gigantica are the causative agents of liver fluke disease (fas- (Clades 3 and 4). Consistent with these observations our ciolosis) in sheep and cattle. Although infections of F. hepat- proteomics studies identified representatives from ica occur predominantly in regions with temperate climates, Clades 1, 2, and 5 but not from Clades 3 and 4 in adult F.
[Show full text]
Evolution, Expression and Meiotic Behavior of Genes Involved in Chromosome Segregation of Monotremes
G C A T T A C G G C A T genes Article Evolution, Expression and Meiotic Behavior of Genes Involved in Chromosome Segregation of Monotremes Filip Pajpach , Linda Shearwin-Whyatt and Frank Grützner * School of Biological Sciences, The University of Adelaide, Adelaide, SA 5005, Australia; fi[email protected] (F.P.); [email protected] (L.S.-W.) * Correspondence: [email protected] Abstract: Chromosome segregation at mitosis and meiosis is a highly dynamic and tightly regulated process that involves a large number of components. Due to the fundamental nature of chromosome segregation, many genes involved in this process are evolutionarily highly conserved, but duplica- tions and functional diversification has occurred in various lineages. In order to better understand the evolution of genes involved in chromosome segregation in mammals, we analyzed some of the key components in the basal mammalian lineage of egg-laying mammals. The chromosome passenger complex is a multiprotein complex central to chromosome segregation during both mitosis and meio- sis. It consists of survivin, borealin, inner centromere protein, and Aurora kinase B or C. We confirm the absence of Aurora kinase C in marsupials and show its absence in both platypus and echidna, which supports the current model of the evolution of Aurora kinases. High expression of AURKBC, an ancestor of AURKB and AURKC present in monotremes, suggests that this gene is performing all necessary meiotic functions in monotremes. Other genes of the chromosome passenger complex complex are present and conserved in monotremes, suggesting that their function has been preserved Citation: Pajpach, F.; in mammals.
[Show full text]
A Core Program of Gene Expression Characterizes Cancer Metastases
www.impactjournals.com/oncotarget/ Oncotarget, 2017, Vol. 8, (No. 60), pp: 102161-102175 Research Paper A core program of gene expression characterizes cancer metastases Franz Hartung1, Yunguan Wang2, Bruce Aronow2 and Georg F. Weber1 1University of Cincinnati Academic Health Center, Cincinnati, OH, USA 2Computational Medicine Center, Cincinnati Children’s Hospital, Cincinnati, OH, USA Correspondence to: Georg F. Weber, email: [email protected] Keywords: metastasis; metabolism; vascularization; extracellular matrix; ion homeostasis Received: July 28, 2017 Accepted: August 31, 2017 Published: November 02, 2017 Copyright: Hartung et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. ABSTRACT While aberrant expression or splicing of metastasis genes conveys to cancers the ability to break through tissue barriers and disseminate, the genetic basis for organ preference in metastasis formation has remained incompletely understood. Utilizing the gene expression profiles from 653 GEO datasets, we investigate whether the signatures by diverse cancers in various metastatic sites display common features. We corroborate the meta-analysis in a murine model. Metastases are generally characterized by a core program of gene expression that induces the oxidative metabolism, activates vascularization/tissue remodeling, silences extracellular matrix interactions, and alters ion homeostasis. This program distinguishes metastases from their originating primary tumors as well as from their target host tissues. Site- selectivity is accomplished through specific components that adjust to the target micro-environment. The same functional groups of gene expression programs are activated in the metastases of B16-F10 cells to various target organs.
[Show full text]
Thesis FINAL
The Role of CD1d-Mediated Lipid Presentation by Regulatory B Cells in Invariant Natural Killer T Cell Suppression of Autoimmunity by Kristine Oleinika Supervisor Professor Claudia Mauri UCL Immunology I, Kristine Oleinika, confirm that the work presented in this thesis is my own. Where information has been derived from other sources, I confirm that this has been indicated in the thesis. Kristine Oleinika Acknowledgements To Professor Claudia Mauri, my supervisor and mentor Throughout my PhD years I have so admired your energy and passion, which has made me fall in love with science over and over again. Thank you for looking after me, your guidance has been invaluable in my journey in both science and life. I am incredibly grateful for being part of the wonderful team that you have gathered around you, scientific debate that you have fostered in the group, and for encouraging the friendships within it. To all my colleagues You have made this such an adventure, sharing my enthusiasm for science, politics and footwear, with you I have always felt like a member of an incredibly, almost insultingly, over-educated and over-loving family. And I apologise for the many times you have had to endure listening to my idea for “PhD: the musical” and late night immunology aphorisms, or being on the receiving end of the impromptu enforced hugs. Lizzy, Diego and Paul – thank you for making me think about immunology, socialism, feminism, literature and art (..) ad infinitum. And for your helpful comments on the thesis. Madhvi, overachieving mama bear, thanks for being a fantastic listener.
[Show full text]
The Roles Played by Highly Truncated Splice Variants of G Protein-Coupled Receptors Helen Wise
Wise Journal of Molecular Signaling 2012, 7:13 http://www.jmolecularsignaling.com/content/7/1/13 REVIEW Open Access The roles played by highly truncated splice variants of G protein-coupled receptors Helen Wise Abstract Alternative splicing of G protein-coupled receptor (GPCR) genes greatly increases the total number of receptor isoforms which may be expressed in a cell-dependent and time-dependent manner. This increased diversity of cell signaling options caused by the generation of splice variants is further enhanced by receptor dimerization. When alternative splicing generates highly truncated GPCRs with less than seven transmembrane (TM) domains, the predominant effect in vitro is that of a dominant-negative mutation associated with the retention of the wild-type receptor in the endoplasmic reticulum (ER). For constitutively active (agonist-independent) GPCRs, their attenuated expression on the cell surface, and consequent decreased basal activity due to the dominant-negative effect of truncated splice variants, has pathological consequences. Truncated splice variants may conversely offer protection from disease when expression of co-receptors for binding of infectious agents to cells is attenuated due to ER retention of the wild-type co-receptor. In this review, we will see that GPCRs retained in the ER can still be functionally active but also that highly truncated GPCRs may also be functionally active. Although rare, some truncated splice variants still bind ligand and activate cell signaling responses. More importantly, by forming heterodimers with full-length GPCRs, some truncated splice variants also provide opportunities to generate receptor complexes with unique pharmacological properties. So, instead of assuming that highly truncated GPCRs are associated with faulty transcription processes, it is time to reassess their potential benefit to the host organism.
[Show full text]
ANTICORPI BT-Policlonali
ANTICORPI BT-policlonali Cat# Item Applications Reactivity Source BT-AP00001 11β-HSD1 Polyclonal Antibody WB,IHC-p,ELISA Human,Mouse,Rat Rabbit BT-AP00002 11β-HSD1 Polyclonal Antibody WB,IHC-p,ELISA Human,Mouse,Rat Rabbit BT-AP00003 14-3-3 β Polyclonal Antibody WB,IHC-p,IF,ELISA Human,Mouse,Rat Rabbit BT-AP00004 14-3-3 β/ζ Polyclonal Antibody WB,IHC-p,ELISA Human,Mouse,Rat Rabbit BT-AP00005 14-3-3 γ Polyclonal Antibody WB,IHC-p,IF,ELISA Human,Mouse,Rat Rabbit BT-AP00006 14-3-3 ε Polyclonal Antibody WB,IHC-p,IF,ELISA Human,Mouse,Rat Rabbit BT-AP00007 14-3-3 ε Polyclonal Antibody WB,IHC-p Mouse,Rat Rabbit BT-AP00008 14-3-3 ζ Polyclonal Antibody WB,IHC-p,ELISA Human,Mouse,Rat Rabbit WB,IHC- BT-AP00009 14-3-3 ζ Polyclonal Antibody p,IP,IF,ELISA Human,Mouse,Rat Rabbit BT-AP00010 14-3-3 ζ/δ Polyclonal Antibody WB,IHC-p,IF,ELISA Human,Mouse,Rat Rabbit BT-AP00011 14-3-3 η Polyclonal Antibody WB,IHC-p,IF,ELISA Human,Mouse,Rat Rabbit BT-AP00012 14-3-3 θ Polyclonal Antibody WB,IHC-p,IF,ELISA Human,Mouse,Rat Rabbit BT-AP00013 14-3-3 θ/τ Polyclonal Antibody WB,IHC-p,IF,ELISA Human,Mouse,Rat Rabbit BT-AP00014 14-3-3 σ Polyclonal Antibody WB,IHC-p,ELISA Human,Mouse Rabbit BT-AP00015 14-3-3-pan (Acetyl Lys51/49) Polyclonal Antibody WB,ELISA Human,Mouse,Rat Rabbit BT-AP00016 17β-HSD11 Polyclonal Antibody WB,ELISA Human Rabbit BT-AP00017 17β-HSD4 Polyclonal Antibody WB,IHC-p,ELISA Human,Mouse,Rat Rabbit BT-AP00018 2A5B Polyclonal Antibody WB,ELISA Human Rabbit BT-AP00019 2A5E Polyclonal Antibody WB,ELISA Human,Mouse Rabbit BT-AP00020 2A5G Polyclonal Antibody
[Show full text]