DF6869-REG3G Antibody

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Affinity Biosciences website:www.affbiotech.com order:[email protected] REG3G Antibody Cat.#: DF6869 Concn.: 1mg/ml Mol.Wt.: 19kDa Size: 100ul,200ul Source: Rabbit Clonality: Polyclonal Application: WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500, ELISA(peptide) 1:20000-1:40000 *The optimal dilutions should be determined by the end user. Reactivity: Human,Mouse,Rat Purification: The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific). Specificity: REG3G Antibody detects endogenous levels of total REG3G. Immunogen: A synthesized peptide derived from Mouse REG3G, corresponding to a region within N-terminal amino acids. Uniprot: O09049 Description: The regeneration (REG) family consists of secretory proteins involved in liver, pancreatic, gastric and intestinal cell proliferation or differentiation. Members of the REG family are divided into four subclasses, designated types I, II, III and IV, all of which share a common gene structure containing five introns and six exons. Members of the Reg family have been implicated in the regulation of cell growth, tumorigenesis and the progression of cancer. Reg lll (regenerating islet-derived 3 gamma), also known as pancreatitis-associated protein 1B, PAP1B, or UNQ429, is a 175 amino acid secreted protein that is expressed almost exclusively in pancreas, with low levels of expression in testis. Reg lll functions as an antimicrobial protein involved in controlling bacterial proliferation and may be induced during acute pancreatitis. The gene encoding Reg lll maps to human chromosome 2, which houses over 1,400 genes and comprises nearly 8% of the human genome. Storage Condition and Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM Buffer: NaCl, 0.02% sodium azide and 50% glycerol.Store at -20 °C.Stable for 12 months from date of receipt. 1 / 2 Affinity Biosciences website:www.affbiotech.com order:[email protected] Western blot analysis of extracts from PC12, using REG3G Antibody. The lane on the left was treated with blocking peptide. DF6869 at 1/200 staining Human colon cancer tissue sections by IHC-P. The tissue was formaldehyde fixed and a heat mediated antigen retrieval step in citrate buffer was performed. The tissue was then blocked and incubated with the antibody for 1.5 hours at 22°C. An HRP conjugated goat anti-rabbit antibody was used as the secondary antibody. DF6869 staining A549 cells by IF/ICC. The samples were fixed with PFA and permeabilized in 0.1% Triton X-100,then blocked in 10% serum for 45 minutes at 25°C. Samples were then incubated with primary Ab(DF6869) and mouse anti-beta tubulin Ab(T0023) for 1 hour at 37°C. An AlexaFluor594 conjugated goat anti-rabbit IgG(H+L) Ab(Red) and an AlexaFluor488 conjugated goat anti-mouse IgG(H+L) Ab(Green) were used as the secondary antibody. IMPORTANT: For western blot, incubate membrane with diluted primary Ab in 5% w/v milk , 1X TBS, 0.1% Tween®20 at 4°C with gentle shaking, overnight. For Research Use Only. Not for use in diagnostic and therapeutic procedures. Not for resale without express authorization. 2 / 2 Powered by TCPDF (www.tcpdf.org).

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B Inhibition in a Mouse Model of Chronic Colitis1
The Journal of Immunology Differential Expression of Inflammatory and Fibrogenic Genes and Their Regulation by NF-␬B Inhibition in a Mouse Model of Chronic Colitis1 Feng Wu and Shukti Chakravarti2 Fibrosis is a major complication of chronic inflammation, as seen in Crohn’s disease and ulcerative colitis, two forms of inflam- matory bowel diseases. To elucidate inflammatory signals that regulate fibrosis, we investigated gene expression changes under- lying chronic inflammation and fibrosis in trinitrobenzene sulfonic acid-induced murine colitis. Six weekly 2,4,6-trinitrobenzene sulfonic acid enemas were given to establish colitis and temporal gene expression patterns were obtained at 6-, 8-, 10-, and 12-wk time points. The 6-wk point, TNBS-w6, was the active, chronic inflammatory stage of the model marked by macrophage, neu- trophil, and CD3؉ and CD4؉ T cell infiltrates in the colon, consistent with the idea that this model is T cell immune response driven. Proinflammatory genes Cxcl1, Ccl2, Il1b, Lcn2, Pla2g2a, Saa3, S100a9, Nos2, Reg2, and Reg3g, and profibrogenic extra- cellular matrix genes Col1a1, Col1a2, Col3a1, and Lum (lumican), encoding a collagen-associated proteoglycan, were up-regulated at the active/chronic inflammatory stages. Rectal administration of the NF-␬B p65 antisense oligonucleotide reduced but did not abrogate inflammation and fibrosis completely. The antisense oligonucleotide treatment reduced total NF-␬B by 60% and down- regulated most proinflammatory genes. However, Ccl2, a proinflammatory chemokine known to promote fibrosis, was not down- regulated. Among extracellular matrix gene expressions Lum was suppressed while Col1a1 and Col3a1 were not. Thus, effective treatment of fibrosis in inflammatory bowel disease may require early and complete blockade of NF-␬B with particular attention to specific proinflammatory and profibrogenic genes that remain active at low levels of NF-␬B.
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