TGFB1 ELISA Kit

Catalog No. ABIN577091

This Colorimetric ELISA kit is designed for the quantitative measurement of Human TGFB1.

Quick Overview for TGFB1 ELISA Kit (ABIN577091)

Target: TGFB1 (Transforming Growth Factor, beta 1 (TGFB1))

Reactivity: Human

Detection Method: Colorimetric

Method Type: Sandwich ELISA

Application: ELISA

Product Details TGFB1 ELISA Kit

Purpose: For the quantitative determination of human Transforming Growth Factor beta1 (TGF-β1) concentrations in serum, plasma, cell culture supernatant, and other biological fluids.

Analytical Method: Quantitative

Components: Standards: 1 set/2 vials

Application Details

Plate: Pre-coated

Restrictions: For Research Use only

Handling

Preservative: Without preservative

Target Details for TGFB1

Target: TGFB1 (Transforming Growth Factor, beta 1 (TGFB1))

Alternative Name: Transforming growth factor beta 1 (TGF-b1)

Background: C-Reactive Protein (CRP) is an acute phase protein, originally identified and named for its ability to precipitate the C-polysaccharide of pneumococcus in the presence of calcium1. It is the prototypic acute phase reactant whose presence in plasma or serum serves as a useful laboratory indicator of systemic inflammatory disease. Normally, CRP in human biological fluids is present in trace amounts (.7-8. mg/L, median .6 mg/L). Stimulated by certain cytokines (IL-1 , IL-1 , TNF- and , and indirectly by IL-6)2,3, its sythesis by hepatocytes enhanced dramatically. Thus during the acute phase response CRP's serum concentration can increase up to 1-fold within a few hours3. Human CRP is a kind of nonimmunoglobulin serum substance, a heat labile -globulin. It is classified in a superfamily of proteins termed pentaxins or pentraxins: cyclic, non- glycosylated structures composed of five apparently identical globular non-covalently linked subunits aggregated symmetrically. Each subunit is 23.5 kD (26 amino acids), with a total molecular weight of 117.5 kDa, and consists of 14 anti-parallel -strands arranged in two -sheets4,7. Among acute phase proteins, CRP is a fast-reacting, sensitive and the most easily measured one. It has a rapid response time, short half life and large incremental change and its catabolism is not affected by the type of inflammation. Moreover, its normalization can monitor the cure process from the disease, hence it has the largest data base of i d sease-released change. CRP can be used as an early and pre-clinical marker of inflammation. Especially in situations where microbiological diagnosis is difficult or too slow in the clinical context, CRP measurements can be used to infer the presence of bacterial infection5. Following acute tissue damage or during the course of infectious and non-infectious diseases, hepatic synthesis of CRP dramatically increases its plasma concentration from .58 (range .6-8.) mg/L to 1-5 mg/L within 24-48 hours. Typically, mild elevations of CRP (1-4 mg/L)6,8 are seen in a variety of inflammatory conditions such as viral infections, rheumatoid arthritis, Crohn's disease, post-transplant rejections, infant septic coxitis (arthritis of the hip joint), and neoplasia, whereas more marked rises (CRP 4->5 mg/L) are usual seen in acute and severe bacterial infections such as acute, severe pancreatitis and appenditis, bacterial or purulent meningitis, aspirition pneumonia, sequela-prone osteomyelitis, osteoarthritis, giant cell arthritis, septicaemia, systemic vasculitis, acute sinusitis, acute otitis media, infected urinary tract obstruction, extensive trauma, fractures, burns, infectious post-operative complications and acute myocardial infarction6,8,9. Combined with IL-6, CRP seems to be a valuable parameter in the early diagnosis of neonatal infections. S7.5(3) CRP 2 _x000C_ Serum amyloid A (SAA) is another major acute phase protein whose response is highly correlated with that of CRP (r=.75-.88, P=.1)1,11. Both CRP and SAA respond sensitively to several stimuli with elevated serum levels including surgical trauma, acute infection and allograft rejection, and show almost similar kinetics in many diseases processes. But they differ in certain responses, e.g., the reactivity and sensitivity of SAA is higher than CRP in viral infection, patients on steroid therapy, chronic allograft rejection. So the combined use of CRP and SAA may distinguish viral from bacterial infection, and may distinguish allograft rejection from infection. Meanwhile, CRP proved more useful than SAA to predict cardiovascular events and monitor process of diseases and the effects of some treatments

Pathways: EGFR Signaling Pathway, Dopaminergic Neurogenesis, Cellular Response to Molecule of Bacterial Origin, Glycosaminoglycan Metabolic Process, Regulation of Leukocyte Mediated Immunity, Regulation of Muscle Cell Differentiation, Positive Regulation of Immune Effector Process, Cell-Cell Junction Organization, Production of Molecular Mediator of Immune Response, Ribonucleoside Biosynthetic Process, Skeletal Muscle Fiber Development, Regulation of Carbohydrate Metabolic Process, Protein targeting to Nucleus, Autophagy, Cancer Immune Checkpoints