Description:

Size: 100ul

Catalog no.: bs-2351R-A594

Price: 380 EUR

Product details

Modification Site

None

Gene ID Number

12876729

Crossreactivity

Bacteria

Tested applications

IF(IHC-P)

French translation

anticorps

Modification

Unmodified

Clonality

Polyclonal

Immunogen range

290-331/331

Excitation emission

590nm/617nm

Target Antigen

E. coli LPS

Concentration

1ug per 1ul

Conjugated with

ALEXA FLUOR® 594

Conjugated

Alexa conjugate 1

Recommended dilutions

IF(IHC-P)(1:50-200)

Clone

Polyclonal antibody

Cross-reactive species details

Escherichia coli O83

Synonyms

Escherichia coli LPS.

Purification

Purified by Protein A.

Conjugation

Alexa Fluor,ALEXA FLUOR® 594

Category

Conjugated Primary Antibodies

Host Organism

Rabbit (Oryctolagus cuniculus)

Also known as

Anti-E. coli LPS PAb ALEXA FLUOR 594

Specificity

This is a highly specific antibody against E. coli LPS.

Long name

E. coli LPS Polyclonal Antibody, ALEXA FLUOR 594 Conjugated

Source

KLH conjugated synthetic peptide derived from Escherichia coli O83:H1 str. NRG 857C Lipopolysaccharides

Storage conditions

Store this antibody in aqueous buffered solution containing 1% BSA, 50% glycerol and 0.09% sodium azide. Keep refrigerated at 2 to 8 degrees Celcius for up to one year.

Properties

For facs or microscopy Alexa 1 conjugate.If you buy Antibodies supplied by Bioss Primary Conjugated Antibodies. ALEXA FLUOR they should be stored frozen at - 24°C for long term storage and for short term at + 5°C.

Background of the antigen

Some form of LPS is a major component of the cell membrane of Gram negative bacteria, contributing greatly to the structural integrity of the bacteria, and protecting the membrane from certain kinds of chemical attack. LPS is an endotoxin, and induces a strong response from normal animal immune systems. LPS function has been under experimental research for several years due to its role in activating many transcriptional factors, which become active after stimulation with LPS. LPS also produces many types of mediators involved in septic shock.

Gene

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.