MOUSE Anti-BURKHOLDERIA MALLEI LPS Antibody

531 EUR

200ug

GEN214575

N/A

N/A

N/A

N/A

N/A

IgG1

3D11

anticorps

Antibodies

Monoclonal

Mus musculus

Mnoclonal antibodies

Mouse (Mus musculus)

BURKHOLDERIA MALLEI LPS

IgG concentration 1.0mg/ml

ELISA (EIA), Western Blot (WB)

Purified (Purified IgG - liquid)

If you buy Antibodies supplied by MBS Monoclonals they should be stored frozen at - 24°C for long term storage and for short term at + 5°C.

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.

Bacterial; Due to limited knowledge and inability for testing each and every species, the reactivity of the antibody may extend to other species which are not listed hereby.

Mouse or mice from the Mus musculus species are used for production of mouse monoclonal antibodies or mabs and as research model for humans in your lab. Mouse are mature after 40 days for females and 55 days for males. The female mice are pregnant only 20 days and can give birth to 10 litters of 6-8 mice a year. Transgenic, knock-out, congenic and inbread strains are known for C57BL/6, A/J, BALB/c, SCID while the CD-1 is outbred as strain.

Store the antibody at +4 degrees Celsius for short-term storage and at -20 degrees Celsius for long-term.Storage in frost-free freezers is not recommended. the antibody should be stored undiluted. Repeated freeze - thaw cycles may denature the peptide chains of the antibody and therefore should be maximally avoided. If there is a precipitate in the vial we recommend you to briefly microcentrifugate it prior to use. Shelf Life: 18 months from date of dispatch.

BURKHOLDERIA MALLEI LPS This item recognises the lipopolysaccharide (LPS) of Burkholderia mallei, a gram-negative non-sporing bacillus. Burkholderia mallei is the causative agent of glanders, an infectious disease found mostly in horses. Glanders is characterised by nodular lesions in the lung and ulcers in the mucous membranes of the respiratory tract. Acute disease can cause death from septicaemia in a few days while chronic disease can linger for months. Humans can be infected through direct contact with an infected animal. In humans the infection may be rapidly fatal. Glanders has been eliminated in North America, Australia and most of Europe, but remains endemic in Asia, Africa, the Middle East and Central and South America. _x000D__x000D_The use of B. mallei as a biological weapon has been reported and as there is currently no vaccine available for either humans or animals it remains a possible target for biological warfare.; Since it is not possible to test each and every species our knowledge on the corss reactivity of the antibodies is limited. This particular antibody might cross react with speacies outside of the listed ones.

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.