Recombinant Mycobacterium Tuberculosis 6 Kda Early Secretory Antigenic Target (ESXA) Protein (His)
Beta LifeScience
SKU/CAT #: BLC-00158P
Greater than 90% as determined by SDS-PAGE.
Recombinant Mycobacterium Tuberculosis 6 Kda Early Secretory Antigenic Target (ESXA) Protein (His)
Beta LifeScience
SKU/CAT #: BLC-00158P
Our products are highly customizable to meet your specific needs. You can choose options such as endotoxin removal, liquid or lyophilized forms, preferred tags, and the desired functional sequence range for proteins. Submitting a written inquiry expedites the quoting process.
Product Overview
| Description | Recombinant Mycobacterium Tuberculosis 6 Kda Early Secretory Antigenic Target (ESXA) Protein (His) is produced by our E.coli expression system. This is a protein fragment. |
| Purity | Greater than 90% as determined by SDS-PAGE. |
| Activity | Not tested. |
| Uniprotkb | P9WNK7 |
| Target Symbol | ESXA |
| Synonyms | (ESAT-6) |
| Species | Mycobacterium tuberculosis (strain ATCC 25618 / H37Rv) |
| Expression System | E.coli |
| Tag | C-6His |
| Target Protein Sequence | WNFAGIEAAASAIQGNVTSIHSLLDEGKQSLTKLAAAWGGSGSEAYQGVQQKWDATATELNNALQNLARTISEAGQAMASTEGNVTGMFA |
| Expression Range | 6-95aa |
| Protein Length | Partial |
| Mol. Weight | 16.2 kDa |
| Research Area | Others |
| Form | Liquid or Lyophilized powder |
| Buffer | Liquid form: default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol. Lyophilized powder form: the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0. |
| Reconstitution | Briefly centrifuged the vial prior to opening to bring the contents to the bottom. Reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL. It is recommended to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. The default final concentration of glycerol is 50%. |
| Storage | 1. Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. 2. Avoid repeated freeze-thaw cycles. 3. Store working aliquots at 4°C for up to one week. 4. In general, protein in liquid form is stable for up to 6 months at -20°C/-80°C. Protein in lyophilized powder form is stable for up to 12 months at -20°C/-80°C. |
| Notes | Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week. |
Target Details
| Target Function | A secreted protein that plays a number of roles in modulating the host's immune response to infection as well as being responsible for bacterial escape into the host cytoplasm. Acts as a strong host (human) T-cell antigen. Inhibits IL-12 p40 (IL12B) and TNF-alpha expression by infected host (mouse) macrophages, reduces the nitric oxide response by about 75%. In mice previously exposed to the bacterium, elicits high level of IFN-gamma production by T-cells upon subsequent challenge by M.tuberculosis, in the first phase of a protective immune response. Higher levels (1.6-3.3 uM) of recombinant protein inhibit IFN-gamma production by host (human) T-cells and also IL-17 and TNF-alpha production but not IL-2; decreases expression of host ATF-2 and JUN transcription factors by affecting T-cell receptors signaling downstream of ZAP70, without cytotoxicity or apoptosis. EsxA inhibits IFN-gamma production in human T-cells by activating p38 MAPK (MAPK14), p38 MAPK is not responsible for IL-17 decrease. Binds host (mouse) Toll-like receptor 2 (TLR2) and decreases host MYD88-dependent signaling; binding to TLR2 activates host kinase AKT and subsequently inhibits downstream activation of NF-kappa-B; the C-terminal 20 residues (76-95) are necessary and sufficient for the TLR2 inhibitory effect. Required for induction of host (human) IL-1B maturation and release by activating the host NLRP3/ASC inflammasome; may also promote access of other tuberculosis proteins to the host cells cytoplasm. Induces IL-8 (CXCL8) expression in host (human) lung epithelial cells. Exogenously applied protein, or protein expressed in host (human and mouse), binds beta-2-microglobulin (B2M) and decreases its export to the cell surface, probably leading to defects in class I antigen presentation by the host cell. Responsible for mitochondrial fragmention, redistribution around the cell nucleus and decreased mitochondrial mass; this effect is not seen until 48 hours post-infection. Able to disrupt artificial planar bilayers in the absence of EsxB (CFP-10). Native protein binds artificial liposomes in the absence but not presence of EsxB and is able to rigidify and lyse them; the EsxA-EsxB complex dissociates at acidic pH, EsxB might serve as a chaperone to prevent membrane lysis. Recombinant protein induces leakage of phosphocholine liposomes at acidic pH in the absence of ExsB, undergoes conformational change, becoming more alpha-helical at acidic pH. The study using recombinant protein did not find dissociation of EsxA-EsxB complex at acidic pH. Involved in translocation of bacteria from the host (human) phagolysosome to the host cytoplasm. Translocation into host cytoplasm is visible 3 days post-infection using cultured human cells and precedes host cell death. Recombinant protein induces apoptosis in host (human) differentiated cell lines, which is cell-line dependent; bacteria missing the ESX-1 locus do not induce apoptosis. Host (human) cells treated with EsxA become permeable to extracellular dye. EsxA and EsxA-EsxB are cytotoxic to pneumocytes. ESX-1 secretion system-induced host (mouse) cell apoptosis, which is probably responsible for infection of new host cells, might be due to EsxA. EsxA induces necrosis in aged neutrophils. May help regulate assembly and function of the type VII secretion system (T7SS). EsxA disassembles pre-formed EccC-EsxB multimers, possibly by making EccC-EsxA-EsxB trimers instead of EccC-EsxB-EsxB-EccC tetramers.; May be critical in pro-bacteria versus pro-host interactions; ESX-1 mediates DNA mediated export (maybe via EsxA). The DNA interacts with host (human) cGAS, leading to cGAMP production and activation of the host STING-TBK-1-IRF-3 signaling pathway that leads to IFN-beta which is thought to be 'pro-bacteria'. Mycobacterial dsDNA also interacts with AIM2-NLRP3-ASC to activate an inflammasome, leading to the 'pro-host' IL-1-beta. |
| Subcellular Location | Secreted. Secreted, cell wall. Host cell surface. Host cytoplasm. Host endoplasmic reticulum. Host cell membrane. |
| Protein Families | WXG100 family, ESAT-6 subfamily |
| Database References | KEGG: mtu:Rv3875 STRING: 83332.Rv3875 |
Gene Functions References
- The authors conclude that Mycobacterium tuberculosis ESAT-6 stimulates macrophage IL-6 production through STAT3 activation. PMID: 28106119
- Rv1057 deletion reduced ESAT-6 secretion and modulated the interactions between M. tuberculosis and macrophages. PMID: 29134265
- Mycobacterium tuberculosis ESAT-6 induces dose-dependent activation of caspase-1, and cytotoxicity in mouse retinal pigment epithelium cells. PMID: 29180292
- Here we engineer the sequence of EsxA to add desirable tryptic properties aimed at improving complex MS analysis. We demonstrate that EsxA variants are amenable to MS analysis and remain functional in established in vitro and ex vivo assays of Esx-1-function. PMID: 27625110
- EsxA contributes to mycobacterial virulence with its membrane-permeabilizing activity that is required for cytosolic translocation. PMID: 27600772
- that ESX-1 [6-kDa early secretory antigenic target (ESAT-6) secretion system 1] dependent cell membrane lysis is contact dependent and accompanied by gross membrane disruptions rather than discrete pores. PMID: 28119503
- ESAT6 may induce renal injury by promoting miR-155 expression through the TLR-4/MyD88 signaling pathway in MTB-infected mice. PMID: 28655852
- This is the first report proclaiming that the ESAT-6 regulates Prdx-1 which is involved in the increase of mycobacterial uptake and survival. The intermediate mechanisms involve the increased Prdx-1 production in macrophages through the activation of p38 and NRF-2 dependent signaling. PMID: 29032183
- ESAT-6, an essential virulence factor of Mycobacterium tuberculosis, may contribute to the abnormal hematopoiesis of tuberculosis patients by inhibiting the proliferation and differentiation of CD34-positive hematopoietic cells via apoptosis. PMID: 27745787
- Mycobacterium bovis bacillus Calmette-Guerin (BCG) vaccine-induced protection was lost in the absence of ESAT-6-dependent cytosolic contact. PMID: 27111234
- ESAT6 can inhibit the autophagy and promote the growth of Mycobacterium tuberculosis. PMID: 28274307
- Mycobacterium tuberculosis activates inflammatory and stromal cells to secrete MMP-10, and this is partly driven by the virulence factor early secretory antigenic 6. PMID: 27654284
- Furthermore, in both Raw264.7 and ACM cells, MTOR inhibition significantly suppressed the survival of BCG. In conclusion, our study highlights how ESAT6 blocks autophagy and promotes BCG survival in a way that activates MTOR. PMID: 27317487
- This study suggests I25-H26 as the pH-sensor essential for Mycobacterium smegmatis ESAT-6 to fully acquire the activity, while multiple residues contributed to Mycobacterium tuberculosis ESAT-6 pore-forming activity. PMID: 26801203
- ESAT-6/ESAT-6:CFP-10 can enter into the endoplasmic reticulum where it sequesters beta2M to inhibit cell surface expression of MHC-I-beta2M complexes, resulting in downregulation of class I-mediated antigen presentation. PMID: 25356553
- ESAT-6 forms dimers/multimers with higher molecular weight, which disappeared under the action of the detergent amidosulfobetaine-14, giving rise to another conformational state of the protein. PMID: 26260636
- MicroRNA profiling of Mtb-infected macrophages revealed the downregulation of miR-let-7f in a manner dependent on the Mtb secreted effector ESAT-6 leading to A20 increase, a feedback inhibitor of the NF-kappaB pathway. PMID: 25683052
- ESAT-6 significantly increased miR-155 expression, which was dependent on TLR2/NF-kappaB activation in macrophages. PMID: 25721573
- ESAT-6 has a leukocidin function, which may facilitate bacterial avoidance of the antimicrobial action of the neutrophil. PMID: 25321481
- Both the N- and C-terminal flexible arms are required for membrane disruption, and the central helix-turn-helix motif of EsxA inserts into the membrane. PMID: 25645924
- Assessment of T cell response to novel Mycobacterium tuberculosis synthetic overlapping peptides mixtures (Rv2659 and Rv2660) and ESAT-6 in Egyptian patients. PMID: 25812354
- Further, activation of nuclear factor-kappaB (NF-kappaB) and the NF-kappaB-regulated genes encoding tumor necrosis factor-alpha (TNF-alpha) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) participated in esxT-induced apoptosis. PMID: 25242740
- These data show Mycobacterium tuberculosis ESAT6-induced down-regulation of IFN-gamma / SOCS1 expression to be induced only in active tuberculosis cases, distinguishing them from healthy individuals likely to have latent tuberculosis. PMID: 24423713
- Two lines of transgenic carrot plants producing Mycobacterium tuberculosis proteins (ESAT6 and CFP10) have been constructed... the proteins in question are appropriate as a candidate edible vaccine against tuberculosis. PMID: 24455687
- MtbESAT-6 possesses a unique membrane-interacting activity that is not found in MsESAT-6. PMID: 23150662
- The virulence-associated secreted protein ESAT-6 plays a key role in miR-155 induction and its subsequent effects on Bach1 and SHIP1 repression. PMID: 22712528
- Mycobacterium tuberculosis-derived protein ESAT-6 (Rv3875) induced transient increase in the expression and release of BAT3 in macrophages. PMID: 22808273
- Hepatitis B virus core particles were capable of enhancing ESAT-6-specific immune responses in a mouse model PMID: 21689705
- ESAT-6 directly inhibits human T-cell responses by affecting TCR signaling pathways downstream of ZAP70. PMID: 20006311
- As virulent Mycobacterium tuberculosis reaches a threshold number of bacilli inside the human macrophageESAT-6-dependent necrosis occurs, activating caspase-1 in the process. PMID: 21637850
- ESAT-6 inhibits T cell IFN-gamma production in a p38 MAPK-dependent manner. PMID: 21586573
- Data show that ESAT-6 test may be the most appropriate for diagnosis of childhood TB, both LTBI and TB disease. PMID: 21039742
- The authors show that recognition of Mycobacterium tuberculosis infection by the NLRP3 inflammasome requires the activity of the bacterial virulence factor ESAT-6, and the subsequent IL-1beta response is regulated by NLR/CARD proteins such as ASC. PMID: 20148899
- Phenylalanine-rich peptides potently bind ESAT6, a virulence determinant of Mycobacterium tuberculosis, which may have a role in the pathogen's growth PMID: 19901982
- These studies demonstrate that ESAT6 causes cytolysis of type 1 and type 2 pneumocytes. PMID: 19906174
- study identified mechanism by which mycobacteria induce granulomas: ESAT-6 induced MMP9 in epithelial cells neighboring infected macrophages; MMP9 enhanced recruitment of macrophages, which contributed to nascent granuloma maturation & bacterial growth PMID: 20007864
- role in pathogenicity and antigenicity of Mycobacterium tuberculosis [review] PMID: 15488391
- treatment of J774 macrophages with ESAT-6 also enhanced IFN-gamma-induced expression of the surface molecules B7.1, Class II Antigen, and Intercellular Adhesion Molecule-1 PMID: 15860216
- The surface features of the ESAT-6.CFP10 complex, together with observed binding to specific host cells, strongly suggest a key signalling role for the complex PMID: 15973432
- A strict correlation has been found between ESAT-6 export and the generation of ESAT-6 specific T-cell responses in mice. PMID: 16368961
- findings demonstrate that ESAT6 induces apoptosis in THP-1 human macrophages; induction of apoptosis by ESAT6 is dependent on the dose of the protein and the expression of caspase genes PMID: 17298391
- Direct binding of ESAT-6 to toll-like receptor 2 activated Akt and prevented interaction between the adaptor MyD88 and 'downstream' kinase IRAK4 PMID: 17486091
- ESAT-6 induced phosphorylation of extracellular signal-regulated kinases 1/2 (ERK1/2) in the cytoplasm but not in the nucleus, which normally is the case for MAP kinases. ESAT-6 also antagonized LPS-induced ERK1/2 phosphorylation in the nucleus. PMID: 17915024
- Results demonstrate that ESAT-6-specific Th1 cells can provide protection against inhaled M. tuberculosis, but only after the first week of infection. PMID: 18779346
- ESAT-6 directly inhibits human T cell responses to mycobacterial antigens by affecting T cell receptor signaling pathways downstream of ZAP70 protein tyrosine kinase. PMID: 19265145
- positive correlation between ESAT6-induced IFNgamma and CXCL9 was present in all tuberculosis patients, but IFNgamma and CCL2 was only correlated in limited disease PMID: 19340290
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