Search results for 15

Sorting Nexin 15 (SNX15) Antibody (Biotin), Abbexa, abx316587

SNX15 Antibody (Biotin) is a Rabbit Polyclonal against SNX15 conjugated to Biotin.

Growth Differentiation Factor 15 (GDF15) Antibody, Abbexa, abx403871

Human Growth Differentiation Factor 15 (GDF15) Antibody is a Mouse monoclonal against Growth Differentiation Factor 15 (GDF15).

Bone Morphogenetic Protein 15 (BMP15) Antibody, Abbexa, abx103113

Polyclonal Antibody to BMP15 (BMP15).

Anti-Histone H3.3 Antibody (N158/15), AntibodySystem, RHN25801

Anti-QKI-7 Antibody (N183/15), AntibodySystem, RHK48205

Anti-Neuroligin-3 Antibody (N110/15), AntibodySystem, RHN20401

Human Protocadherin 15 (PCDH15) ELISA Kit, Abbexa, abx152866

Human Protocadherin 15 (PCDH15) ELISA Kit is an ELISA Kit for the in vitro quantitative measurement of Human Protocadherin 15 (PCDH15) concentrations in tissue homogenates, cell lysates and other biological fluids. This assay has high sensitivity and excellent specificity for detection of Protocadherin 15 (PCDH15)No significant cross-reactivity or interference between Protocadherin 15 (PCDH15) and analogues was observed.

Activated C3, Human, mAb I3/15, Hycult Biotech, HM2257

C3 itself is a pivotal 190 kD protein central to the complement system, integral to the classical, alternative, and lectin pathways of complement activation. Notably, its synthesis is tissue-specific and responds dynamically to various stimulatory agents. Being the most abundant complement system protein, with serum levels around 1.3 mg/ml, C3’s activation is a key event in immune response. Activation of C3, a critical step identified by the activated C3 antibody, involves its cleavage into C3a and C3b. C3a plays a vital role in mediating local inflammatory processes, with notable anaphylatoxic properties. It induces smooth muscle contraction, increases vascular permeability, and triggers histamine release from mast cells and basophils. Conversely, C3b attaches to immune complexes and undergoes further cleavage into iC3b, C3c, C3dg, and C3f. Collectively, these fragments are known as activated C3 (act. C3). The most significant function of these C3 fragments is their interaction with other immune cells. The neo-epitopes formed during activation, which the activated C3 antibody detects, are vital for understanding the complement cascade’s impact on the immune system. Monoclonal antibodies like I3/15, which target these neo-epitopes, have become essential tools for directly quantifying activation at different steps of the complement cascade. Studying the activated C3 antibody’s role in C3 activation is key for immune response insights and therapies. Not sure which C3 antibody to use? With numerous options available, it is essential to select the right C3 antibody to ensure the success of your research. We designed a guide to assist you in making an informed decision: Go to our C3 researcher’s guide and choose the right antibody

C1-INH, Human, clone 15/12, Hycult Biotech, HM2411

Mouse monoclonal antibody HM2411 recognizes human C1-inhibitor. The complement system plays important roles in both innate and adaptive immune response and can produce an inflammatory and protective reaction to challenges from pathogens before an adaptive response can occur. There are three pathways of complement activation. The classical pathway (CP) is initiated by Immune complexes; the lectin pathway (LP) by surface bound mannan binding lectin; and the alternative (AP) by all the surfaces that are not specifically protected against it. Each generates a C3 convertase, a serine protease that cleaves the central complement protein C3, and generates the major cleavage fragment C3b. The C3 and C5 convertases are enzymatic complexes that initiate and amplify the activity of the complement pathways and ultimately generate the cytolytic MAC (C5b-9). C1 inhibitor (C1-INH) is a heavily glycosylated single chain molecule of 500 AA. It inhibits multiple enzymes, including C1s&r of the CP and MASP-1&2 of the LP, plasmin in the fibrinolytic system and Factor XIIa&XIa of the contact and coagulation system. C1-INH is also called C1 esterase inhibitor, due C1s is often cleaved by synthetic esters in spectrophotometry. C1-INH plays an important role in suppression of inflammation and vascular permeability. C1-INH binding of C1 to the catalytic site of both C1r and C1s releases the latter two from the complex. As a result the activation of the complement system is blocked. Binding to MASP blocks function and thereby consumption of C2,3&4. C1-INH spares the AP, leaving part of the innate antibacterial defense intact. Besides, C1-INH can directly bind and neutralize LPS, inhibiting sepsis and endotoxin shock. C1-INH administration is the common treatment for hereditary angioedema (HAE). A disease commonly caused by heterozygous deficiency of C1-INH and leading to low levels of functional C1-INH and recurrent episodes of dermal and submucosal swelling. This is mediated by its ability to control activation of the contact system in inhibiting bradykinin generation and thereby control of vascular permeability.

C7, Human, mAb WU 4-15, Hycult Biotech, HM2277

The monoclonal antibody WU 4-15 recognizes C7, one of the components of the terminal complement complex (TCC), also know as the membrane attack complex (MAC). Proteolytic cleavage of C5 by C5 convertase generates C5b which initiates assembly of the C5b-9 MAC. This complex is assembled from five precursor molecules in the serum, finalized with the polymerization of C9 which accompanies insertion of the complex into the cell membrane causing cellular lysis. C7 occupies an important position in the TCC cascade. C7 undergoes a hydrophilic-amphiphilic transition following activation. It enables the developing MAC to bind directly to target cell membranes. C7 has been shown to exhibit genetic polymorphism. Polymorphonuclear leukocytes represent a major source of C7. The fact that inflammatory cells have the potential to secrete C7 suggests an important role for locally produced complement in the inflammatory process. The monoclonal antibody WU 4-15 identifies an specific allotype of C7: C7 M. 62% of the caucasians is homozygous for C7 M, 31% heterozygous. Antibody Wu 4-15 enables to quantify the contribution of locally synthesized C7 to the inflammatory process and to identify the allotype.