IKBKB Polyclonal Antibody

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IKBKB polyclonal antibody Gene Summary: NFKB1 (MIM 164011) or NFKB2 (MIM 164012) is bound to REL (MIM 164910), RELA (MIM Catalog Number: PAB18155 164014), or RELB (MIM 604758) to form the NFKB complex. The NFKB complex is inhibited by I-kappa-B Regulatory Status: For research use only (RUO) proteins (NFKBIA, MIM 164008, or NFKBIB, MIM 604495), which inactivate NF-kappa-B by trapping it in Product Description: Rabbit polyclonal antibody raised the cytoplasm. Phosphorylation of serine residues on the against synthetic peptide of IKBKB. I-kappa-B proteins by kinases (IKBKA, MIM 600664, or IKBKB) marks them for destruction via the ubiquitination Immunogen: A synthetic peptide corresponding to pathway, thereby allowing activation of the NF-kappa-B human IKBKB. complex. Activated NFKB complex translocates into the nucleus and binds DNA at kappa-B-binding motifs such Host: Rabbit as 5-prime GGGRNNYYCC 3-prime or 5-prime Reactivity: Human,Mouse,Rat HGGARNYYCC 3-prime (where H is A, C, or T; R is an A or G purine; and Y is a C or T pyrimidine).[supplied by Applications: ELISA, IHC-P, WB-Ce OMIM] (See our web site product page for detailed applications information) References: 1. NIBP, a novel NIK and IKK(beta)-binding protein that Protocols: See our web site at enhances NF-(kappa)B activation. Hu WH, Pendergast http://www.abnova.com/support/protocols.asp or product JS, Mo XM, Brambilla R, Bracchi-Ricard V, Li F, Walters page for detailed protocols WM, Blits B, He L, Schaal SM, Bethea JR. J Biol Chem. 2005 Aug 12;280(32):29233-41. Epub 2005 Jun 10. Specificity: This antibody is specific to IKBKB. 2. IKK beta plays an essential role in the phosphorylation of RelA/p65 on serine 536 induced by Form: Liquid lipopolysaccharide. Yang F, Tang E, Guan K, Wang CY. J Immunol. 2003 Jun 1;170(11):5630-5. Purification: Affinity purification 3. IKK beta is required for Bcl-2-mediated NF-kappa B activation in ventricular myocytes. Regula KM, Ens K, Concentration: 1 mg/mL Kirshenbaum LA. J Biol Chem. 2002 Oct Recommend Usage: Western Blot (1:500-1:1000) 11;277(41):38676-82. Epub 2002 Aug 7. Immunohistochemistry (1:50-1:100) ELISA (1:5000) The optimal working dilution should be determined by the end user. Storage Buffer: In PBS, 150mM NaCl, pH 7.4 (50% glycerol, 0.02% sodium azide) Storage Instruction: Store at -20°C. Aliquot to avoid repeated freezing and thawing. Entrez GeneID: 3551 Gene Symbol: IKBKB Gene Alias: FLJ40509, IKK-beta, IKK2, IKKB, MGC131801, NFKBIKB Page 1/1 Powered by TCPDF (www.tcpdf.org).

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Gprc5b Modulates Inflammatory Response in Glomerular Diseases
BASIC RESEARCH www.jasn.org GPRC5b Modulates Inflammatory Response in Glomerular Diseases via NF-kB Pathway Sonia Zambrano,1 Katja Möller-Hackbarth,1 Xidan Li,1 Patricia Q. Rodriguez,1 Emmanuelle Charrin,1 Angelina Schwarz,1 Jenny Nyström,2 Annika Östman Wernerson,3 Mark Lal,4 and Jaakko Patrakka1 1Karolinska Insitutet/AstraZeneca Integrated Cardio Metabolic Center, Department of Laboratory Medicine, Karolinska Institutet at Karolinska University Hospital Huddinge, Stockholm, Sweden; 2Department of Physiology, Institute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden; 3Division of Renal Medicine, Department of Clinical Sciences, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden; and 4Division of Bioscience, Department of Cardiovascular, Renal and Metabolic Diseases, Innovative Medicines Biotech Unit, AstraZeneca, Gothenburg, Sweden ABSTRACT Background Inflammatory processes play an important role in the pathogenesis of glomerulopathies. Finding novel ways to suppress glomerular inflammation may offer a new way to stop disease progression. However, the molecular mechanisms that initiate and drive inflammation in the glomerulus are still poorly understood. Methods We performed large-scale gene expression profiling of glomerulus-associated G protein– coupled receptors (GPCRs) to identify new potential therapeutic targets for glomerulopathies. The expression of Gprc5b in disease was analyzed using quantitative PCR and immunofluorescence, and by analyzing published microarray data sets. In vivo studies were carried out in a podocyte-specificGprc5b knockout mouse line. Mechanistic studies were performed in cultured human podocytes. Results We identified an orphan GPCR, Gprc5b, as a novel gene highly enriched in podocytes that was significantly upregulated in common human glomerulopathies, including diabetic nephropathy, IgA ne- phropathy, and lupus nephritis. Similar upregulation of Gprc5b was detected in LPS-induced nephropathy in mice.
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Genome-Wide Sirna Screen for Mediators of NF-Κb Activation
Genome-wide siRNA screen for mediators SEE COMMENTARY of NF-κB activation Benjamin E. Gewurza, Fadi Towficb,c,1, Jessica C. Marb,d,1, Nicholas P. Shinnersa,1, Kaoru Takasakia, Bo Zhaoa, Ellen D. Cahir-McFarlanda, John Quackenbushe, Ramnik J. Xavierb,c, and Elliott Kieffa,2 aDepartment of Medicine and Microbiology and Molecular Genetics, Channing Laboratory, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA 02115; bCenter for Computational and Integrative Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114; cProgram in Medical and Population Genetics, The Broad Institute of Massachusetts Institute of Technology and Harvard, Cambridge, MA 02142; dDepartment of Biostatistics, Harvard School of Public Health, Boston, MA 02115; and eDepartment of Biostatistics and Computational Biology and Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02115 Contributed by Elliott Kieff, December 16, 2011 (sent for review October 2, 2011) Although canonical NFκB is frequently critical for cell proliferation, (RIPK1). TRADD engages TNFR-associated factor 2 (TRAF2), survival, or differentiation, NFκB hyperactivation can cause malig- which recruits the ubiquitin (Ub) E2 ligase UBC5 and the E3 nant, inflammatory, or autoimmune disorders. Despite intensive ligases cIAP1 and cIAP2. CIAP1/2 polyubiquitinate RIPK1 and study, mammalian NFκB pathway loss-of-function RNAi analyses TRAF2, which recruit and activate the K63-Ub binding proteins have been limited to specific protein classes. We therefore under- TAB1, TAB2, and TAB3, as well as their associated kinase took a human genome-wide siRNA screen for novel NFκB activa- MAP3K7 (TAK1). TAK1 in turn phosphorylates IKKβ activa- tion pathway components. Using an Epstein Barr virus latent tion loop serines to promote IKK activity (4).
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Supplementary Materials
Supplementary materials Supplementary Table S1: MGNC compound library Ingredien Molecule Caco- Mol ID MW AlogP OB (%) BBB DL FASA- HL t Name Name 2 shengdi MOL012254 campesterol 400.8 7.63 37.58 1.34 0.98 0.7 0.21 20.2 shengdi MOL000519 coniferin 314.4 3.16 31.11 0.42 -0.2 0.3 0.27 74.6 beta- shengdi MOL000359 414.8 8.08 36.91 1.32 0.99 0.8 0.23 20.2 sitosterol pachymic shengdi MOL000289 528.9 6.54 33.63 0.1 -0.6 0.8 0 9.27 acid Poricoic acid shengdi MOL000291 484.7 5.64 30.52 -0.08 -0.9 0.8 0 8.67 B Chrysanthem shengdi MOL004492 585 8.24 38.72 0.51 -1 0.6 0.3 17.5 axanthin 20- shengdi MOL011455 Hexadecano 418.6 1.91 32.7 -0.24 -0.4 0.7 0.29 104 ylingenol huanglian MOL001454 berberine 336.4 3.45 36.86 1.24 0.57 0.8 0.19 6.57 huanglian MOL013352 Obacunone 454.6 2.68 43.29 0.01 -0.4 0.8 0.31 -13 huanglian MOL002894 berberrubine 322.4 3.2 35.74 1.07 0.17 0.7 0.24 6.46 huanglian MOL002897 epiberberine 336.4 3.45 43.09 1.17 0.4 0.8 0.19 6.1 huanglian MOL002903 (R)-Canadine 339.4 3.4 55.37 1.04 0.57 0.8 0.2 6.41 huanglian MOL002904 Berlambine 351.4 2.49 36.68 0.97 0.17 0.8 0.28 7.33 Corchorosid huanglian MOL002907 404.6 1.34 105 -0.91 -1.3 0.8 0.29 6.68 e A_qt Magnogrand huanglian MOL000622 266.4 1.18 63.71 0.02 -0.2 0.2 0.3 3.17 iolide huanglian MOL000762 Palmidin A 510.5 4.52 35.36 -0.38 -1.5 0.7 0.39 33.2 huanglian MOL000785 palmatine 352.4 3.65 64.6 1.33 0.37 0.7 0.13 2.25 huanglian MOL000098 quercetin 302.3 1.5 46.43 0.05 -0.8 0.3 0.38 14.4 huanglian MOL001458 coptisine 320.3 3.25 30.67 1.21 0.32 0.9 0.26 9.33 huanglian MOL002668 Worenine
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NFKBIB & FBXW11 Protein Protein Interaction Antibody Pair Catalog # : DI0194 規格 : [ 1 Set ] List All Specification Application Image Product This protein protein interaction antibody pair set comes with two In situ Proximity Ligation Assay (Cell) Description: antibodies to detect the protein-protein interaction, one against the NFKBIB protein, and the other against the FBXW11 protein for use in in situ Proximity Ligation Assay. See Publication Reference below. Reactivity: Human Quality Control Protein protein interaction immunofluorescence result. Testing: Representative image of Proximity Ligation Assay of protein-protein interactions between NFKBIB and FBXW11. HeLa cells were stained with anti-NFKBIB rabbit purified polyclonal antibody 1:1200 and anti- FBXW11 mouse monoclonal antibody 1:50. Each red dot represents the detection of protein-protein interaction complex. The images were analyzed using an optimized freeware (BlobFinder) download from The Centre for Image Analysis at Uppsala University. Supplied Antibody pair set content: Product: 1. NFKBIB rabbit purified polyclonal antibody (20 ug) 2. FBXW11 mouse monoclonal antibody (40 ug) *Reagents are sufficient for at least 30-50 assays using recommended protocols. Storage Store reagents of the antibody pair set at -20°C or lower. Please aliquot Instruction: to avoid repeated freeze thaw cycle. Reagents should be returned to - Page 1 of 4 2016/5/19 20°C storage immediately after use. MSDS: Download Publication Reference 1. An analysis of protein-protein interactions in cross-talk pathways reveals CRKL as a novel prognostic marker in hepatocellular carcinoma. Liu CH, Chen TC, Chau GY, Jan YH, Chen CH, Hsu CN, Lin KT, Juang YL, Lu PJ, Cheng HC, Chen MH, Chang CF, Ting YS, Kao CY, Hsiao M, Huang CY.
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UNIVERSITY of CALIFORNIA Los Angeles Dissecting the Regulatory
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REGULAR ARTICLE Insights into the genomic landscape of MYD88 wild-type Waldenstrom¨ macroglobulinemia Zachary R. Hunter,1,2 Lian Xu,1 Nickolas Tsakmaklis,1 Maria G. Demos,1 Amanda Kofides,1 Cristina Jimenez,1 Gloria G. Chan,1 Jiaji Chen,1 Xia Liu,1 Manit Munshi,1 Joshua Gustine,1 Kirsten Meid,1 Christopher J. Patterson,1 Guang Yang,1,2 Toni Dubeau,1 Mehmet K. Samur,2,3 Jorge J. Castillo,1,2 Kenneth C. Anderson,2,3 Nikhil C. Munshi,2,3 and Steven P. Treon1,2 1Bing Center for Waldenstrom¨ ’s Macroglobulinemia, Dana-Farber Cancer Institute, Boston, MA; 2Harvard Medical School, Boston, MA; and 3Jerome Lipper Myeloma Center, Dana-Farber Cancer Institute, Boston, MA Activating MYD88 mutations are present in 95% of Waldenstrom¨ macroglobulinemia (WM) Key Points patients, and trigger NF-kB through BTK and IRAK. The BTK inhibitor ibrutinib is active • MUT Mutations affecting in MYD88-mutated (MYD88 ) WM patients, but shows lower activity in MYD88 wild-type k WT WT NF- B, epigenomic (MYD88 ) disease. MYD88 patients also show shorter overall survival, and increased regulation, or DNA risk of disease transformation in some series. The genomic basis for these findings remains damage repair were to be clarified. We performed whole exome and transcriptome sequencing of sorted tumor identified in MYD88 WT samples from 18 MYD88 patients and compared findings with WM patients with wild-type WM. MUT MYD88 disease. We identified somatic mutations predicted to activate NF-kB(TBL1XR1, • k NF- B pathway muta- PTPN13, MALT1, BCL10, NFKB2, NFKBIB, NFKBIZ, and UDRL1F), impart epigenomic tions were downstream dysregulation (KMT2D, KMT2C, and KDM6A), or impair DNA damage repair (TP53, ATM, and of BTK, and many TRRAP).
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Oncogene (2006) 25, 3247–3257 & 2006 Nature Publishing Group All rights reserved 0950-9232/06 $30.00 www.nature.com/onc ORIGINAL ARTICLE The human homologue of the RNA polymerase II-associated factor 1 (hPaf1), localized on the 19q13 amplicon, is associated with tumorigenesis N Moniaux1,4, C Nemos1,4, BM Schmied2, SC Chauhan1, S Deb1, K Morikane2, A Choudhury1, M VanLith2, M Sutherlin2, JM Sikela3, MA Hollingsworth1,2 and SK Batra1,2 1Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, USA; 2Eppley Institute, University of Nebraska Medical Center, Omaha, NE, USA and 3Department of Pharmacology, University of Colorado Health Sciences Center, Denver, CO, USA The 19q13 amplicon in pancreatic cancer cells contains a somes, chromosomal translocations, and gene amplifi- novel pancreatic differentiation 2 (PD2) gene (accession cations, induce a transformed phenotype leading to number AJ401156), which was identified by differential cancer. These genetic alterations constitute key events screening analysis. PD2 is the human homologue of the contributing to tumor progression and metastasis. They RNA polymerase II-associated factor 1 (hPaf1). In yeast, are often stabilized when they confer a growth or Paf1 is part of the transcription machinery, acting as a survivaladvantage to the cells(Lengauer et al., 1998). docking protein in between the complexes Rad6-Bre1, Gene amplification (HSR, homogeneously staining COMPASS-Dot1p, and the phosphorylated carboxyl region and DM, double minute) is one of the most terminal domain of the RNA polymerase II. As such, important mechanisms leading to the alteration of gene Paf1 is directly involved in transcription elongation via expression in solid tumors.
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First Insight Into the Modulation of Noncanonical NF-Κb Signaling
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Computational Simulations to Predict Creatine Kinase-Associated Factors: Protein-Protein Interaction Studies of Brain and Muscle Types of Creatine Kinases
SAGE-Hindawi Access to Research Enzyme Research Volume 2011, Article ID 328249, 12 pages doi:10.4061/2011/328249 Research Article Computational Simulations to Predict Creatine Kinase-Associated Factors: Protein-Protein Interaction Studies of Brain and Muscle Types of Creatine Kinases Wei-Jiang Hu,1 Sheng-Mei Zhou,2 Joshua SungWoo Yang,3, 4 and Fan-Guo Meng1 1 Zhejiang Provincial Key Laboratory of Applied Enzymology, Yangtze Delta Region Institute of Tsinghua University, Jiaxing 314006, China 2 College of Biology and Chemical Engineering, Jiaxing University, Jiaxing 314001, China 3 Korean Bioinformation Center (KOBIC), Korea Research Institute of Bioscience & Biotechnology (KRIBB), Daejeon 305-806, Republic of Korea 4 Department of Bioinformatics, University of Sciences & Technology, Daejeon 205-305, Republic of Korea Correspondence should be addressed to Fan-Guo Meng, [email protected] Received 17 May 2011; Accepted 26 May 2011 Academic Editor: Jun-Mo Yang Copyright © 2011 Wei-Jiang Hu 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. Creatine kinase (CK; EC 2.7.3.2) is related to several skin diseases such as psoriasis and dermatomyositis. CK is important in skin energy homeostasis because it catalyzes the reversible transfer of a phosphoryl group from MgATP to creatine. In this study, we predicted CK binding proteins via the use of bioinformatic tools such as protein-protein interaction (PPI) mappings and suggest the putative hub proteins for CK interactions. We obtained 123 proteins for brain type CK and 85 proteins for muscle type CK in the interaction networks.
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