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Monoclonal Antibody Ihc-Leica® bond™ Regulation of Bone Resorption

$269
100 µl
APPLICATIONS
REACTIVITY
Human

Application Methods: IHC-Leica® Bond™, Immunohistochemistry (Paraffin), Western Blotting

Background: Macrophage-colony stimulating factor (M-CSF, CSF-1) receptor is an integral membrane tyrosine kinase encoded by the c-fms proto-oncogene. M-CSF receptor is expressed in monocytes (macrophages and their progenitors) and drives growth and development of this blood cell lineage. (1-3). Binding of M-CSF to its receptor induces receptor dimerization, activation, and autophosphorylation of cytoplasmic tyrosine residues used as docking sites for SH2-containing signaling proteins (4). There are at least five major tyrosine autophosphorylation sites. Tyr723 (Tyr721 in mouse) is located in the kinase insert (KI) region. Phosphorylated Tyr723 binds the p85 subunit of PI3 kinase as well as PLCγ2 (5). Phosphorylation of Tyr809 provides a docking site for Shc (5). Overactivation of this receptor can lead to a malignant phenotype in various cell systems (6). The activated M-CSF receptor has been shown to be a predictor of poor outcome in advanced epithelial ovarian carcinoma (7) and breast cancer (8).

$129
20 µl
$303
100 µl
APPLICATIONS
REACTIVITY
Human

Application Methods: IHC-Leica® Bond™, Immunohistochemistry (Paraffin), Western Blotting

Background: Cyclic ADP-ribose hydrolase 1 (CD38) is a transmembrane protein involved in several important biological processes, including immune response, insulin secretion, and social behavior. Originally described as a glycosylated immune cell surface marker, additional research determined that CD38 is a multifunctional enzyme that catalyzes the synthesis and hydrolysis of cyclic ADP ribose (cADPR) from NAD (1,2). Under acidic conditions, CD38 also catalyzes the synthesis of nicotinic acid adenine dinucleotide phosphate (NAADP) from NADP+. Both cADPR and NAADP act as calcium ion mobilizing messengers that target different intracellular Ca2+ stores (3-6). Since CD38 is the primary mammalian NAD+ glycohydrolase responsible for NAD+ metabolism, CD38 may be a valuable therapeutic target for treatment of metabolic diseases regulated by NAD+-dependent pathways (7,8). CD38 has also been considered a possible therapeutic target for antibody-mediated therapy for myeloma and chronic lymphocytic leukemia (9-11).