Products_type

Protein

Tissue

control

Description

The LITAF (Lipopolysaccharide- TNF factor, CMT1C, FLJ38636, MGC116698, MGC116700, MGC116701, MGC125274, MGC125275, MGC125276, PIG7, SIMPLE, TP53I7, LPS- TNF-alpha factor) (Control Peptide)[LITAF] is a α- or alpha protein sometimes glycoprotein present in blood.Isotype or positive controls by peptides, antibodies and deactivated samples.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.Peptides short amino acid chains or epitopes or blocking antagonists. The shortest peptides are dipeptides, consisting of 2 amino acids joined by a single peptide bond, followed by tripeptides, tetra peptides, ... till polypeptides that are long, continuous, and unbranched synthetic peptide chains. These biological oligomers and polymers can be Solid-phase peptide synthesis (SPPS), or in continue produced for custom peptide synthesis projects. The High-efficiency solid phase peptide synthesis (HE-SPPS) is give very low production costs.

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.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.