M. Tuberculosis 48 kDa protein (DAGA-191)

M. Tuberculosis 48 kDa protein, Recombinant protein from E. coli for ELISA

Product Overview
Mycobacterium tuberculosis (MTB) is a pathogenic bacterial species in the genus Mycobacterium and the causative agent of most cases of tuberculosis. The physiology of M. tuberculosis is highly aerobic and requires high levels of oxygen. Primarily a pathogen of the mammalian respiratory system, MTB infects the lungs and is the causative agent of tuberculosis. - See more at: https://www.fitzgerald-fii.com/mycobacterium-tuberculosis-48-kda-protein-30-am74.html#sthash.MbZsx7Wh.dpuf
Molecular Weight
48 kDa
Alternative Names
M. Tuberculosis 63 kDa protein; Mycobacterium tuberculosis 103 kDa protein; Mycobacterium tuberculosis; M. tuberculosis; MTB; TB antigen
> 95% pure
Batch dependent - please inquire should you have specific requirements.
1 mg
25mM Tris-Cl, 0.1% SDS, pH 8.3
Store at 4 ℃ for short term storage. Aliquot and store at -20 ℃ for long term storage. Avoid repeated freeze/thaw cycles. - See more at: https://www.fitzgerald-fii.com/mycobacterium-tuberculosis-48-kda-protein-30-am74.html#sthash.MbZsx7Wh.dpuf
Antigen Description
Mycobacterium tuberculosis is an obligate pathogenic bacterial species in the family Mycobacteriaceae and the causative agent of tuberculosis First discovered in 1902 by Robert Koch, M. tuberculosis has an unusual, waxy coating on its cell surface (primar
M. Tuberculosis 63 kDa protein;Mycobacterium tuberculosis 103 kDa protein;Mycobacterium tuberculosis;M. tuberculosis;MTB;TB antigen


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In vitro activity of Melaleuca cajuputi against mycobacterial species


Authors: Bua, Alessandra; Molicotti, Paola; Donadu, Matthew Gavino; Usai, Donatella; Le, Lam Son; Thi Trung Thu Tran; Viet Quynh Tram Ngo; Marchetti, Mauro; Usai, Marianna; Cappuccinelli, Piero; Zanetti, Stefania

The increasing incidence of resistance in tuberculosis and in atypical mycobacterial infections has prompted the search for alternative agents. We explored the antimycobacterial activity of Melaleuca cajuputi essential oil against tubercular and non tubercular mycobacterials isolates. The good activity observed towards M. cajuputi indicated that this essential oil might represent a promising antimicrobial agents, particularly in the management of microbial resistance.

DNA hypermethylation during tuberculosis dampens host immune responsiveness


Authors: Dinardo, Andrew R.; Rajapakshe, Kimal; Nishiguchi, Tomoki; Grimm, Sandra L.; Mtetwa, Godwin; Dlamini, Qiniso; Kahari, Jaquiline; Mahapatra, Sanjana; Kay, Alexander; Maphalala, Gugu; Mace, Emily M.; Makedonas, George; Cirillo, Jeffrey D.; Netea, Mihai G.; Van Crevel, Reinout; Coarfa, Cristian; Mandalakas, Anna M.

Mycobacterium tuberculosis (M. tuberculosis) has coevolved with humans for millennia and developed multiple mechanisms to evade host immunity. Restoring host immunity in order to improve outcomes and potentially shorten existing therapy will require identification of the full complement by which host immunity is inhibited. Perturbation of host DNA methylation is a mechanism induced by chronic infections such as HIV, HPV, lymphocytic choriomeningitis virus (LCMV), and schistosomiasis to evade host immunity. Here, we evaluated the DNA methylation status of patients with tuberculosis (TB) and their asymptomatic household contacts and found that the patients with TB have DNA hypermethylation of the IL-2/STAT5, TNF/NF-kappa B, and IFN-gamma signaling pathways. We performed methylation-sensitive restriction enzyme-quantitative PCR (MSRE-qPCR) and observed that multiple genes of the IL-12/IFN-gamma signaling pathway (IL12B, IL12RB2, TYK2, IFNGR1, JAK1, and JAK2) were hypermethylated in patients with TB. The DNA hypermethylation of these pathways was associated with decreased immune responsiveness with decreased mitogen-induced upregulation of IFN-gamma, TNF, IL-6, CXCL9, CXCL10, and IL-1 beta production. The DNA hypermethylation of the IL-12/IFN-gamma pathway was associated with decreased IFN-gamma-induced gene expression and decreased IL-12-inducible upregulation of IFN-gamma. This study demonstrates that immune cells from patients with TB are characterized by DNA hypermethylation of genes critical to mycobacterial immunity resulting in decreased mycobacteria-specific and nonspecific immune responsiveness.

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