LITAF (Lipopolysaccharide-induced TNF factor, CMT1C, FLJ38636, MGC116698, MGC116700, MGC116701, MGC125274, MGC125275, MGC125276, PIG7, SIMPLE, TP53I7, LPS-induced TNF-alpha factor) Antibody

531 EUR

100ul

GEN608501

N/A

IgG1

LITAF

10C307

anticorps

Antibodies

Monoclonal

Human (Homo sapiens)

Mnoclonal antibodies

Mouse (Mus musculus)

ELISA (EL/EIA), Western Blot (WB)

Affinity Purified by immunoaffinity chromatography.

Supplied as a liquid in PBS, pH 7.4, 0.1% sodium azide.

LITAF; LITAF; PIG7; SIMPLE; TP53I7; FLJ38636; MGC116698; MGC116700; MGC116701; MGC125274; MGC125275; MGC125276; PIG7; SIMPLE

LITAF; LITAF; PIG7; SIMPLE; TP53I7; FLJ38636; MGC116698; MGC116700; MGC116701; MGC125274; MGC125275; MGC125276; PIG7; SIMPLE

LITAF; LITAF; PIG7; SIMPLE; TP53I7; FLJ38636; MGC116698; MGC116700; MGC116701; MGC125274; MGC125275; MGC125276; PIG7; SIMPLE

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.

Human (Homo sapiens); 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.

Recognizes recombinant human LITAF. ; 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.

Store the antibody at +4 degrees Celsius for short term storage.. For long-term storage and to avoid repeated freezing and thawing, add sterile 40-50% glycerol, aliquot and For optimal long term storage, the antibody should be kept at -20 degrees Celsius. Aliquots are stable for at least 12 months the antibody should be stored at -20 degrees Celsius.. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Further dilutions can be made in assay buffer.

lipopolysaccharide-induced tumor necrosis factor-alpha factor isoform 2; Lipopolysaccharide-induced tumor necrosis factor-alpha factor; lipopolysaccharide-induced tumor necrosis factor-alpha factor; p53-induced gene 7 protein; LPS-induced TNF-alpha factor; tumor protein p53 inducible protein 7; lipopolysaccharide-induced TNF-alpha factor; small integral membrane protein of lysosome/late endosome; lipopolysaccharide-induced TNF factor; Small integral membrane protein of lysosome/late endosome; p53-induced gene 7 protein

The LITAF (Lipopolysaccharide- TNF factor, CMT1C, FLJ38636, MGC116698, MGC116700, MGC116701, MGC125274, MGC125275, MGC125276, PIG7, SIMPLE, TP53I7, LPS- TNF-alpha factor) Antibody is a α- or alpha protein sometimes glycoprotein present in blood.Aplha, transcription related growth factors and stimulating factors or repressing nuclear factors are complex subunits of proteins involved in cell differentiation. Complex subunit associated factors are involved in hybridoma growth, Eosinohils, eritroid proliferation and derived from promotor binding stimulating subunits on the DNA binding complex. NFKB 105 subunit for example is a polypetide gene enhancer of genes in B cells.Induced protein genes, factors or kinases, increase the production of (an enzyme or other protein) at the level of genetic transcription.

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.Tumor necrosis factor (TNFa, tumor necrosis factor alpha, TNFα, cachexin, or cachectin) is a cell signaling protein (cytokine) involved in systemic inflammation and is one of the cytokines that make up the acute phase reaction. It is produced chiefly by activated macrophages, although it can be produced by many other cell types such as CD4+ lymphocytes, NK cells, neutrophils, mast cells, eosinophils, and neurons. TNFb or TNF beta also bin on TNF receptors for Th1 activation.