目录号 | 产品详情 | 靶点 | |
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TN1545 | Tyrosinase | ||
D-Tyrosine, the D-isomer of tyrosine, acts as a negative regulator of melanin synthesis by inhibiting tyrosinase activity. Furthermore, D-Tyrosine also inhibits biofilm formation and induces the self-dispersal of biofilms, while not affecting bacterial growth. | |||
T36735 | Reactive Oxygen Species Antifungal | ||
3,5-Di-tert-butylphenol 诱导活性氧物质的积累。 3,5-Di-tert-butylphenol 具有抗生物膜和抗真菌活性。 | |||
T1305 | Antibacterial Antibiotic | ||
Ceftazidime (GR20263) 是可静脉内或肌肉给药的第头孢菌素。它对革兰氏阳性和革兰氏阴性需氧细菌有体外活性。它对肠杆菌科特别有效,对大多数 β-内酰胺酶具有抗水解作用。 | |||
T8507 | Antibacterial | ||
MAC-545496 是一种抗毒剂,可逆转耐甲氧西林的菌株中的 β-内酰胺耐药性。它是糖肽抗性相关蛋白 R 的纳摩尔抑制剂,对全长 GraR 蛋白具有很强的结合亲和力。 | |||
T3S2340 | Others Antibacterial | ||
Usaramine (Mucronatine) 是从 Crolatalaria pallida 种子中分离得到的一种吡咯里嗪类生物碱。它对 Lactuca sativa var 具有植物毒性。 | |||
T3S1319 | Others Antifungal | ||
(+)-Magnoflorine (Thalictrin) 是从 Acoruscalamus 中分到的一种阿朴啡生物碱,可以减少 C. albicans 生物膜的形成,具有抗真菌、抗氧化、抗糖尿病、镇静和抗焦虑的作用。 | |||
T3S1320 | Others Antifungal | ||
(+)-Magnoflorine iodide (Thalictrine iodide) 是从 Acoruscalamus 中分到的一种阿朴啡生物碱,具有抗炎、抗真菌、抗氧化和抗糖尿病的作用,可以减少C. albicans 生物膜的形成。 | |||
T4S1321 | Others Antifungal | ||
(+)-Magnoflorine chloride (Escholine chloride) 是从 Acoruscalamus 中分到的一种阿朴啡生物碱,具有抗炎、抗真菌、抗氧化和抗糖尿病的作用,可以减少 C. albicans 生物膜的形成。 | |||
T18408 | Antibacterial | ||
N-Butanoyl-L-homoserine lactone (C4-HSL) 是一种可降解的 ADClinker,用于抗体偶联药物的合成。它可用于抗菌生物膜,具有抗菌活性。它的适配体抑制铜绿假单胞菌生物膜的形成,可用于阻止群体感应。 | |||
TQ0251 | Others | ||
(Z)-2-decenoic acid (cis-dec-2-enoic acid) 是一种由铜绿假单胞菌产生的不饱和脂肪酸。它能够诱导一系列革兰氏阴性细菌(包括铜绿假单胞菌)和革兰氏阳性细菌形成的生物膜发生分散反应。它能够抑制生物膜发育。 |
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-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-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-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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