TRAP Recombinant Rabbit mAb (一抗) - IHC-P,IHC-F,IF | Bioss

bsm-61758R

重组兔单抗

TRAP Recombinant Rabbit mAb

抗酒石酸酸性磷酸酶5型/5型酸性磷酸酶重组兔单抗

HPAP; TRACP5a; TRACP5b; TRAP; TRAcP; TrATPase; PPA5_HUMAN; ACP5; TR-AP; Tartrate-resistant acid ATPase (TrATPase); Type 5 acid phosphatase; 3.1.3.2; acid phosphatase 5, tartrate resistant; tartrate-resistant acid phosphatase; human purple acid phosphatase

Rabbit

A synthesized peptide derived from human TRAP: 150-325

IgG

Liquid

affinity purified by Protein A

Recombinant

2D12

37 kDa

37 kDa

10mM phosphate buffered saline(pH 7.4) with 150mM sodium chloride, 0.05% BSA, 0.02% Proclin300 and 50% glycerol.

Store at 4℃ for short term. Store at -20℃ for long term. Avoid repeated freeze/thaw cycles.

This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.

抗酒石酸盐酸性磷酸酶(Tartrate-Resistant Acid Phosphatase,TRAP)是破骨细胞功能的重要标志物,它的活性与破骨细胞活性呈正相关.

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.

ACP5

Tartrate-resistant acid phosphatase type 5

Exists either as monomer or, after proteolytic processing, as a dimer of two chains linked by disulfide bond(s).

Lysosome.

Defects in ACP5 are the cause of spondyloenchondrodysplasia with immune dysregulation (SPENCDI) [MIM:607944]. 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. Note=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.

Defects in ACP5 are the cause of spondyloenchondrodysplasia with immune dysregulation (SPENCDI) [MIM:607944]. 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. Note=ACP5 inactivating mutations result in a functional excess of phosphorylated osteopontin causing deregulation of osteopontin signaling and consequential autoimmune disease.