ulcerative

p63 Protein, Human, Recombinant (His) is expressed in E. coli expression system with N-6xHis tag. The predicted molecular weight is 80.8 kDa and the accession number is Q9H3D4.

The molecular features at the IL19 locus may modestly alter the establishment of HIV-1 infection. Interleukin (IL) 19, IL-20, and IL-24 belong to the IL-10 cytokine family and have been identified to play a role in the regulation of epidermal functions and inflammation. The expression of IL19 in biopsies of patients with active ulcerative colitis was increased compared with patients with quiescent ulcerative colitis and that colitis was attenuated in IL-19-deficient mice. The disruption of the epithelial barrier with dextran sodium sulfate leads to increased IL-19 expression. Attenuated colitis in IL-19-deficient animals was associated with reduced numbers of IL-6-producing macrophages in the inflamed colonic lamina propria. Microbial-driven expression of IL-19 by intestinal macrophages may contribute to the pathogenesis of inflammatory bowel disease.

Blood vessel epicardial substance (BVES), or POPDC1, is a tight junction-associated transmembrane protein that modulates epithelial-to-mesenchymal transition (EMT) via junctional signaling pathways. BVES plays a protective role both in ulcerative and infectious colitis and identify BVES as a critical protector of colonic mucosal integrity. The Popeye domain containing1, also called Bves (Popdc1/Bves), is a transmembrane protein that functions in muscle regeneration, heart rate regulation, hypoxia tolerance, and ischemia preconditioning. The expression of Popdc1/Bves is elevated in cardiomyocytes maintained in serum free defined medium. Popdc1/Bves plays a role in the preservation of cardiomyocyte viability under serum deficiency through the alteration of Rac1 activity and the regulation of Bnip3 expression by FoxO3 and NFκB transcription factors pointing to Popdc1/Bves as a potential target to enhance heart protection. Blood vessel epicardial substance (BVES) is a tight junction-associated protein that regulates epithelial-mesenchymal states and is underexpressed in epithelial malignancy. Loss of BVES promotes inflammatory tumourigenesis through dysregulation of Wnt signalling and the oncogene c-Myc. BVES promoter methylation status may serve as a CAC biomarker. Blood vessel epicardial substance (BVES/Popdc1) is a junctional-associated transmembrane protein that is underexpressed in a number of malignancies and regulates epithelial-to-mesenchymal transition. BVES is a key regulator of intestinal stem cell programs and mucosal homeostasis.

Sialate O-acetylesterase belongs to the family of hydrolases, specifically those acting on carboxylic ester bonds. It is widely expressed with high expression in the testis, prostate, and colon. The systematic name of this enzyme class is N-acyl-O-acetylneuraminate O-acetylhydrolase. Other names in common use include N-acetylneuraminate acetyltransferase, sialate 9(4)-O-acetylesterase, and sialidase. Sialate O-acetylesterase catalyzes the removal of O-acetyl ester groups from position 9 of the parent sialic acid, N-acetylneuraminic acid. Defects in Sialate O-acetylesterase are a cause of autoimmune disease type 6 (AIS6). Individuals manifesting susceptibility to autoimmune disease type 6 can suffer from juvenile idiopathic arthritis, rheumatoid arthritis, multiple sclerosis, Sjogren syndrome, systemic lupus erythematosus, type 1 diabetes, ulcerative colitis, and Crohn disease.

Butyrophilin-like 2 (BTNL2) is a member of the BTN/MOG Ig-superfamily and functions as a negative regulator of immune cell activation. Mouse BTNL2 is type I transmembrane glycoprotein that contains an extracellular domain (ECD), a transmembrane region and a short cytoplasmic domain. The ECD features two V-type Ig-like domains, two C-type Ig-like domains, and four glycosylation sites. BTNL2 is expressed in epithelial cells of the small intestine, colonic dendritic cells, and in cells of the lymph node. BTNL2 expression is upregulated in T cells following activation, a characteristic BTNL2 shares with the homologous B7 family of costimulatory molecules. BTNL2 negatively regulates T cells by inhibiting proliferation and inflammatory cytokine secretion. It also increases the expression of FoxP3 in T cells to promote regulatory T cell development. Single nucleotide polymorphisms in BTNL2 are associated with a risk for sporadic prostate cancer, rheumatoid arthritis, sarcoidosis, ulcerative colitis, and other inflammatory diseases.

ADAM17 is a member of the ADAM protein family of disintegrins and metalloproteases. ADAM17 is ubiquitously expressed in the human colon, with increased activity in the colonic mucosa of patients with ulcerative colitis, a main form of inflammatory bowel disease. The expression of ADAM17 may be inhibited by ethanol. It is involved in the processing of tumor necrosis factor alpha (TNF-α) at the surface of the cell, and from within the intracellular membranes of the trans-Golgi network. ADAM17 also plays a role in the release of a diverse variety of membrane-anchored cytokines, cell adhesion molecules, receptors, ligands, and enzymes. ADAM17 may play a prominent role in the Notch signaling pathway, during the proteolytic release of the Notch intracellular domain (from the Notch1 receptor) that occurs following ligand binding.

IL-32 is a recently discovered cytokine that induces various proinflammatory cytokines (TNF-alpha, IL-1beta, IL-6) and chemokines in both human and mouse cells through the NF-kappaB and p38 MAPK inflammatory signal pathways. It is regulated robustly by other major proinflammatory cytokines and is crucial to inflammation and immune responses. Four of the IL-32 isoforms (alpha, beta, gamma, and delta) are the most representative IL-32 transcripts, and the gamma isoform of IL-32 is the most active, although all isoforms are biologically active. IL-32, a cytokine produced mainly by T, natural killer, and epithelial cells induces significant amounts of TNFalpha and MIP-2 and increases the production of both cytokines in a dose-dependent manner. IL-32 has been implicated in inflammatory disorders, Mycobacterium tuberculosis infections, inflammatory bowel disease, and influenza A virus infection, as well as in some autoimmune diseases, such as rheumatoid arthritis, ulcerative colitis, and in the human stomach cancer, human lung cancer, and breast cancer tissues. Thus, IL-32 expression might be valuable as a biomarker for cancer.