Human Anti-B. pertussis antigens (Pertussis toxin, FHA and LPS) IgG ELISA kit
348 EUR
48 WELLS
ED4280hu-48
This antibody needs to be stored at + 4°C in a fridge short term in a concentrated dilution. Freeze thaw will destroy a percentage in every cycle and should be avoided.
E05 478 566 350 170 or Enzyme-Linked Immunosorbent Assays,E05 478 566 350 170 or Enzyme-Linked Immunosorbent Assays,Human proteins, cDNA and human recombinants are used in human reactive ELISA kits and to produce anti-human mono and polyclonal antibodies. Modern humans (Homo sapiens, primarily ssp. Homo sapiens sapiens). Depending on the epitopes used human ELISA kits can be cross reactive to many other species. Mainly analyzed are human serum, plasma, urine, saliva, human cell culture supernatants and biological samples.
ELISA Enzyme-linked immunosorbent assays Code 90320007 SNOMED
Immunoglobulin gamma, IgG, mouse monoclonal H&L chain clones or rabbit, goat polyclonal antibodies have 4 parts. There are 2 heavy chains, 2 light chains. The IgG antibody has 2 antigen binding sites. They represent 70% or more of serum antibodies. This antibody can be antigen purified or protein A or G purified. For storage sodium azide is added or you can call us to request azide free antibody preparations. These will need colder storage temperatures.
IgG
Bacterial pathogen lipopolysaccharides (LPS) are the major outer surface membrane components present in almost all Gram-negative bacteria and act as extremely strong stimulators of innate or natural immunity in diverse eukaryotic species ranging from insects to humans. LPS consist of a poly- or oligosaccharide region that is anchored in the outer bacterial membrane by a specific carbohydrate lipid moiety termed lipid A. The lipid A component is the primary immunostimulatory center of LPS. With respect to immunoactivation in mammalian systems, the classical group of strongly agonistic (highly endotoxin) forms of LPS has been shown to be comprised of a rather similar set of lipid A types. In addition, several natural or derivative lipid A structures have been identified that display comparatively low or even no immunostimulation for a given mammalian species. Some members of the latter more heterogeneous group are capable of antagonizing the effects of strongly stimulatory LPS/lipid A forms. Agonistic forms of LPS or lipid A trigger numerous physiological immunostimulatory effects in mammalian organisms, but--in higher doses--can also lead to pathological reactions such as the induction of septic shock. Cells of the myeloid lineage have been shown to be the primary cellular sensors for LPS in the mammalian immune system. During the past decade, enormous progress has been obtained in the elucidation of the central LPS/lipid A recognition and signaling system in mammalian phagocytes. According to the current model, the specific cellular recognition of agonistic LPS/lipid A is initialized by the combined extracellular actions of LPS binding protein (LBP), the membrane-bound or soluble forms of CD14 and the newly identified Toll-like receptor 4 (TLR4)*MD-2 complex, leading to the rapid activation of an intracellular signaling network that is highly homologous to the signaling systems of IL-1 and IL-18. The elucidation of structure-activity correlations in LPS and lipid A has not only contributed to a molecular understanding of both immunostimulatory and toxic septic processes, but has also re-animated the development of new pharmacological and immuno-stimulatory strategies for the prevention and therapy of infectious and malignant diseases.
