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pneumococcal

" in TargetMol Product Catalog
  • Inhibitors & Agonists
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PsaA Protein, S. pneumoniae, Recombinant (His & Myc)
Manganese ABC transporter substrate-binding lipoprotein PsaA,psaA,Pneumococcal surface adhesin A
TMPH-03591
Part of an ABC transporter complex involved in manganese import. PsaA Protein, S. pneumoniae, Recombinant (His & Myc) is expressed in E. coli expression system with N-10xHis and C-Myc tag. The predicted molecular weight is 39.9 kDa and the accession number is P42363.
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20 days
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PsaA Protein, S. oralis, Recombinant (His & Myc)
Manganese ABC transporter substrate-binding lipoprotein PsaA,Pneumococcal surface adhesin A,psaA
TMPH-03589
Part of an ATP-driven transport system. PsaA Protein, S. oralis, Recombinant (His & Myc) is expressed in E. coli expression system with N-10xHis and C-Myc tag. The predicted molecular weight is 40.1 kDa and the accession number is Q9L5W9.
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20 days
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PsaA Protein, S. pneumoniae (strain ATCC BAA-255/R6), Recombinant (His & Myc)
psaA,Manganese ABC transporter substrate-binding lipoprotein PsaA,Pneumococcal surface adhesin A
TMPH-03590
Part of an ATP-driven transport system. PsaA Protein, S. pneumoniae (strain ATCC BAA-255 R6), Recombinant (His & Myc) is expressed in E. coli expression system with N-10xHis and C-Myc tag. The predicted molecular weight is 40.0 kDa and the accession number is P0A4G3.
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20 days
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IRAK4 Protein, Human, Recombinant (His)
IPD1,NY-REN-64,REN64,interleukin-1 receptor-associated kinase 4,IRAK-4
TMPY-04483
Interleukin-1 receptor-associated kinase 4, also known as Renal carcinoma antigen NY-REN-64, IRAK-4, and IRAK4, is a member of the protein kinase superfamily, TKL Ser Thr protein kinase family, and Pelle subfamily. IRAK4 contains one death domain and one protein kinase domain. IRAK4 is required for the efficient recruitment of IRAK1 to the IL-1 receptor complex following IL-1 engagement, triggering intracellular signaling cascades leading to transcriptional up-regulation and mRNA stabilization. It also phosphorylates IRAK1. A member of the IL-1 receptor (IL-1R)-associated kinase (IRAK) family, IRAK4, has been shown to play an essential role in Toll-like receptor (TLR)-mediated signaling. IL-1-mediated IRAK4 kinase activity in T cells is essential for the induction of IL-23R expression, Th17 differentiation, and autoimmune disease. Pharmacological blocking of IRAK4 kinase activity will retain some levels of host defense while reducing the levels and duration of inflammatory responses, which should provide beneficial therapies for sepsis and chronic inflammatory diseases. Defects in IRAK4 are the cause of recurrent isolated invasive pneumococcal disease type 1 (IPD1) which is defined as two episodes of IPD occurring at least 1 month apart, whether caused by the same or different serotypes or strains. Recurrent IPD occurs in at least 2% of patients in most series, making IPD the most important known risk factor for subsequent IPD. Defects in IRAK4 are also the cause of IRAK4 deficiency which causes extracellular pyogenic bacterial and fungal infections in otherwise healthy children.
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7-10 days
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Vitronectin Protein, Human, Recombinant (Truncated, His)
Vitronectin,Complement S-protein,Serum Spreading Factor,epibolin,Somatomedin B,Serum-spreading factor,S-protein,V75,VN,VTN,VNT
TMPJ-00472
Vitronectin, also known as VTN, is a large glycoprotein found in blood and the extracellular matrix (ECM). Vitronectin is a plasma glycoprotein implicated as a regulator of diverse physiological process, including blood coagulation, fibrinolysis, pericellular proteolysis, complement dependent immune responses, and cell attachment and spreading. Blocking of Hic(a member of the pneumococcal surface protein C (PspC) family) by specific antiserum or genetic deletion significantly reduced pneumococcal binding to soluble and immobilised vitronectin and to Factor H, respectively. In addition, Vitronectin interact with glycosaminoglycans and proteoglycans. Is recognized by certain members of the integrin family and serves as a cell-to-substrate adhesion molecule. Inhibitor of the membrane-damaging effect of the terminal cytolytic complement pathway.
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7-10 days
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