ELISA/assay

Rat Tartrate Resistant Acid Phosphatase 5B ELISA Kit

MBS031793

48-Strip-Wells

435 USD

ELISA Kit

Rat Tartrate Resistant Acid Phosphatase 5B ELISA Kit

Tartrate Resistant Acid Phosphatase 5B

tartrate-resistant acid phosphatase type 5; Tartrate-resistant acid phosphatase type 5; tartrate-resistant acid phosphatase type 5; TrATPase; tartrate-resistant acid ATPase; acid phosphatase 5, tartrate resistant; Tartrate-resistant acid ATPase; TrATPase; Type 5 acid phosphatase

TRACP-5B

ACP5; ACP5; TRAP; SPENCDI; TR-AP; TrATPase

PPA5_HUMAN

Rat

325

Store all reagents at 2-8 degree C

Assay Type: Sandwich

161377455

NP_001104506.1

NM_001111036.1

P13686

36,599 Da

Defective AMN Causes Hereditary Megaloblastic Anemia 1 Pathway (906000); Defective BTD Causes Biotidinase Deficiency Pathway (906015); Defective CD320 Causes Methylmalonic Aciduria Pathway (906012); Defective CUBN Causes Hereditary Megaloblastic Anemia 1 Pathway (906001); Defective GIF Causes Intrinsic Factor Deficiency Pathway (906004); Defective HLCS Causes Multiple Carboxylase Deficiency Pathway (906014); Defective LMBRD1 Causes Methylmalonic Aciduria And Homocystinuria Type CblF Pathway (906003); Defective MMAA Causes Methylmalonic Aciduria Type CblA Pathway (906010); Defective MMAB Causes Methylmalonic Aciduria Type CblB Pathway (906009); Defective MMACHC Causes Methylmalonic Aciduria And Homocystinuria Type CblC Pathway (906005)

This gene encodes an iron containing glycoprotein which catalyzes the conversion of orthophosphoric monoester to alcohol and orthophosphate. It is the most basic of the acid phosphatases and is the only form not inhibited by L(+)-tartrate. [provided by RefSeq, Aug 2008]

ACP5: Involved in osteopontin/bone sialoprotein dephosphorylation. Its expression seems to increase in certain pathological states such as Gaucher and Hodgkin diseases, the hairy cell, the B-cell, and the T-cell leukemias. Defects in ACP5 are the cause of spondyloenchondrodysplasia with immune dysregulation (SPENCDI). A disease characterized by vertebral and metaphyseal dysplasia, spasticity with cerebral calcifications, and strong predisposition to autoimmune diseases. The skeletal dysplasia is characterized by radiolucent and irregular spondylar and metaphyseal lesions that represent islands of chondroid tissue within bone. ACP5 inactivating mutations result in a functional excess of phosphorylated osteopontin causing deregulation of osteopontin signaling and consequential autoimmune disease. Belongs to the metallophosphoesterase superfamily. Purple acid phosphatase family. Protein type: Cofactor and Vitamin Metabolism - riboflavin; EC 3.1.3.2; Phosphatase; Motility/polarity/chemotaxis. Chromosomal Location of Human Ortholog: 19p13.2. Cellular Component: lysosome; integral to membrane; cytosol. Molecular Function: acid phosphatase activity; ferric iron binding; ferrous iron binding. Biological Process: negative regulation of interleukin-12 production; vitamin metabolic process; negative regulation of nitric oxide biosynthetic process; response to lipopolysaccharide; negative regulation of tumor necrosis factor production; negative regulation of superoxide release; negative regulation of interleukin-1 beta production; riboflavin metabolic process; defense response to Gram-positive bacterium; dephosphorylation; response to cytokine stimulus; negative regulation of inflammatory response; water-soluble vitamin metabolic process; bone resorption. Disease: Spondyloenchondrodysplasia With Immune Dysregulation

48-Strip-Wells

435 USD

96-Strip-Wells

600