目录号 | 产品详情 | 靶点 | |
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T80123 | |||
CRAMP (mouse)为一种抗菌肽,主要应用于探究生物膜相关感染。 | |||
T79555 | |||
G43-C3-TEG为糖基转移酶抑制剂,其作用机制在于降低EPS(细胞外多糖)的生成,进而减少生物膜形成。 | |||
T37555 | |||
Cardanol triene is a phenol found in cashew nut shell liquid that reversibly inhibits tyrosinase with an IC50 value of 40.5 μM in vitro. A mixture of cardanol mono-, di-, and triene is used to synthesize cardanol-metal complexes that inhibit uropathogenic E. coli biofilm formation. | |||
T13947 | Others | ||
Tween 80 是一种非离子型的表面活性剂和乳化剂。Tween 80 可以减少细菌附着并抑制生物膜的形成。Tween 80 可以有效提高化合物在水相中的溶解度,因此被广泛用作药理学实验中的助溶剂。 | |||
T74820 | |||
Antibacterial agent 142 是一种芳香族酰肼,具有抗菌活性。Antibacterial agent 142 具有抑菌作用,抑制生物膜形成。 | |||
TN5466 | |||
Boeravinone B, a novel efflux pump inhibitor, apart from inhibiting the MdeA mediated efflux, also significantly inhibit the biofilm formation of S. aureus, boeravinone B may be used in combination with mupirocin for further development. Boeravinone B exh | |||
T74272 | |||
Antibacterial agent 84 是一种抗真菌化合物。Antibacterial agent 84 以 CNB1 依赖性方式抑制念珠菌。Antibacterial agent 84 抑制C. albicans 生物膜的活性。 | |||
T60610 | |||
LasR-IN-4 是 LasR 的有效抑制剂,可抑制铜绿假单胞菌及其生物膜的形成、绿脓素和鼠李糖脂的产生。 | |||
T71813 | |||
Cardanol diene is a phenol found in cashew nut shell liquid that inhibits tyrosinase with an IC50 value of 52.5 μM in vitro. Cardanol diene is also used to synthesize cardanol-metal complexes that inhibit uropathogenic E. coli biofilm formation. | |||
T61366 | |||
F-17 is a promising virulence factor inhibitor, displaying substantial inhibitory effects on biofilm formation, elastase activity, pyocyanin production, and swarming motility. Additionally, F-17 exhibits a strong binding affinity towards LasR and PqsR. Notably, F-17 does not exhibit any discernible cytotoxicity [1]. |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPH-00712 | PGAB Protein, E. coli, Recombinant (His & Myc) | E. coli | E. coli | ||
Catalyzes the N-deacetylation of poly-beta-1,6-N-acetyl-D-glucosamine (PGA), a biofilm adhesin polysaccharide. N-deacetylation promotes PGA export through the PgaA porin.
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TMPH-00589 | SpoT Protein, E. coli, Recombinant (His & Myc) | E. coli | E. coli | ||
In eubacteria ppGpp (guanosine 3'-diphosphate 5'-diphosphate) is a mediator of the stringent response which coordinates a variety of cellular activities in response to changes in nutritional abundance. This enzyme catalyzes both the synthesis and degradation of ppGpp. The second messengers ppGpp and c-di-GMP together control biofilm formation in response to translational stress; ppGpp represses biofilm formation while c-di-GMP induces it. ppGpp activates transcription of CsrA-antagonistic small RNAs CsrB and CsrC, which downregulate CsrA's action on translation during the stringent response.
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TMPH-03587 | GspB Protein, S. gordonii, Recombinant (GST) | Streptococcus gordonii | E. coli | ||
Plays a role in virulence and host-pathogen interactions. Mediates binding to human platelets via interaction with the human cell surface glycoprotein GP1BA. Plays a positive role in biofilm formation, possibly by self-association via the basic region (BR).
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TMPH-03569 | IcaB Protein, S. aureus, Recombinant (His & Myc) | Staphylococcus aureus | E. coli | ||
Catalyzes the N-deacetylation of poly-beta-1,6-N-acetyl-D-glucosamine (PNAG, also referred to as PIA), a biofilm adhesin polysaccharide. N-deacetylation is crucial for attachment of the polysaccharide to the bacterial cell surface; it leads to the introduction of positive charges in the otherwise neutral PIA polymer, allowing electrostatic interactions.
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TMPH-00331 | ALS3 Protein, Candida albicans, Recombinant (B2M & His & Myc) | Candida albicans | E. coli | ||
Cell surface adhesion protein which mediates both yeast-to-host tissue adherence and yeast aggregation. Plays an important role in the biofilm formation and pathogenesis of C.albicans infections. Necessary for C.albicans to bind to N-cadherin on endothelial cells and E-cadherin on oral epithelial cells and subsequent endocytosis by these cells. During disseminated infection, mediates initial trafficking to the brain and renal cortex and contributes to fungal persistence in the kidneys.
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TMPH-03157 | Fimbrillin Protein, Porphyromonas gingivalis, Recombinant (His & Myc) | Porphyromonas gingivalis | E. coli | ||
Structural subunit of the major fimbriae. These long, filamentous pili are attached to the cell surface; they mediate biofilm formation, adhesion onto host cells and onto other bacteria that are part of the oral microbiome. They play an important role in the invasion of periodontal tissues. Fimbriae and their constituents are major virulence factors. FimA proteins from different strains have highly divergent sequences, and this has been used for classification. The sequence-based classification correlates with pathogenicity.
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TMPH-00337 | HWP1 Protein, Candida albicans, Recombinant (His) | Candida albicans | E. coli | ||
Major hyphal cell wall protein which plays a role of adhesin and is required for mating, normal hyphal development, cell-to-cell adhesive functions necessary for biofilm integrity, attachment to host, and virulence. Promotes interactions with host and bacterial molecules, thus leading to effective colonization within polymicrobial communities. Plays a crucial role in gastrointestinal colonization, in mucosal symptomatic and asymptomatic infections, in vaginitis, as well as in lethal oroesophageal candidiasis, caused by the combined action of fungal virulence factors and host inflammatory responses when protective immunity is absent.
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TMPH-03571 | WalK Protein, S. aureus, Recombinant (His & Myc) | Staphylococcus aureus | E. coli | ||
Member of the two-component regulatory system WalK/WalR that regulates genes involved in cell wall metabolism, virulence regulation, biofilm production, oxidative stress resistance and antibiotic resistance via direct or indirect regulation of autolysins. Functions as a sensor protein kinase which is autophosphorylated at a histidine residue in the dimerization domain and transfers its phosphate group to the conserved aspartic acid residue in the regulatory domain of WalR. In turn, WalR binds to the upstream promoter regions of the target genes to positively and negatively regulate their expression.
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TMPH-00338 | PRA1 Protein, Candida albicans, Recombinant (His) | Candida albicans | Yeast | ||
Cell surface protein involved in the host-parasite interaction during candidal infection. With MP65, represents a major component of the biofilm matrix. Sequesters zinc from host tissue and mediates leukocyte adhesion and migration. As a surface protein, binds the two human complement regulators CFH and CFHR1, as well as plasminogen PLG, mediates complement evasion and extra-cellular matrix interaction and/or degradation. As a released protein, enhances complement control in direct vicinity of the yeast and thus generates an additional protective layer which controls host complement attack, assisting the fungus in escaping host surveillance. Binds to host fluid-phase C3 and blocks cleavage of C3 to C3a and C3b, leading to inhibition of complement activation. Mediates also human complement control and complement evasion through binding to C4BPA, another human complement inhibitor, as well as through binding to host integrin alpha-M/beta-2. Decreases complement-mediated adhesion, as well as uptake of C.albicans by human macrophages.
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TMPH-00617 | MazF Protein, E. coli, Recombinant (His) | E. coli | Yeast | ||
Toxic component of a type II toxin-antitoxin (TA) system. A sequence-specific endoribonuclease it inhibits protein synthesis by cleaving mRNA and inducing bacterial stasis. It is stable, single-strand specific with mRNA cleavage independent of the ribosome, although translation enhances cleavage for some mRNAs. Cleavage occurs at the 5'-end of ACA sequences, yielding a 2',3'-cyclic phosphate and a free 5'-OH, although cleavage can also occur on the 3'-end of the first A. Digests 16S rRNA in vivo 43 nts upstream of the C-terminus; this removes the anti-Shine-Dalgarno sequence forming a mixed population of wild-type and 'stress ribosomes'. Stress ribosomes do not translate leader-containing mRNA but are proficient in translation of leaderless mRNA, which alters the protein expression profile of the cell; MazF produces some leaderless mRNA. The toxic endoribonuclease activity is inhibited by its labile cognate antitoxin MazE. Toxicity results when the levels of MazE decrease in the cell, leading to mRNA degradation. This effect can be rescued by expression of MazE, but after 6 hours in rich medium overexpression of MazF leads to programmed cell death. MazF-mediated cell death occurs following a number of stress conditions in a relA-dependent fashion and only when cells are in log phase; sigma factor S (rpoS) protects stationary phase cells from MazF-killing. Cell growth and viability are not affected when MazF and MazE are coexpressed. Both MazE and MazE-MazF bind to the promoter region of the mazE-mazF operon to inhibit their own transcription. MazE has higher affinity for promoter DNA in the presence of MazF. Cross-talk can occur between different TA systems, ectopic expression of this toxin induces transcription of the relBEF TA system operon with specific cleavage of the mRNA produced.; Might also serve to protect cells against bacteriophage; in the presence of MazE-MazF fewer P1 phages are produced than in a disrupted strain. For strain K38 most wild-type cells are killed but not by phage lysis; it was suggested that MazE-MazF causes P1 phage exclusion from the bacterial population. This phenomenon is strain dependent.; The physiological role of this TA system is debated. Programmed cell death (PCD) occurs when cells are at high density and depends on the presence of MazE-MazF and a quorum sensing pentapeptide, the extracellular death factor (EDF) with sequence Asn-Asn-Trp-Asn-Asn (NNWNN), probably produced from the zwf gene product glucose-6-phosphate 1-dehydrogenase. Cell death governed by the MazE-MazF and DinJ-YafQ TA systems seems to play a role in biofilm formation, while MazE-MazF is also implicated in cell death in liquid media. Implicated in hydroxy radical-mediated cell death induced by hydroxyurea treatment. In conjunction with EDF prevents apoptotic-like death (ALD) in the presence of DNA damaging agents, probably by reducing recA mRNA levels in a non-endonuclease-mediated manner. Other studies (in strains BW25113 and MC4100, the latter makes EDF) demonstrate MazF does not cause PCD but instead bacteriostasis and possibly a dormant state as well as persister cell generation.
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