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high expression of ACP5 correlates with tumor progression and may serve as a potential prognostic biomarker in lung AD.
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TRACP-5b level is significantly associated with the OPG level and with the severity and extent of coronary atherosclerosis in coronary artery disease patients
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Adipokine tartrate-resistant acid phosphatase 5a (TRAP 5a) serum levels correlated positively to anthropometric obesity parameters but not to metabolic syndrome risk factors, indicating that serum TRAP 5a is associated with pathological adipose tissue expansion.
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TRAP promotes metastasis-related cell properties in MDA-MB-231 breast cancer cells via TGFbeta2/TbetaR and CD44, thereby identifying a potential signaling mechanism associated to TRAP action in breast cancer cells.
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Serum TRAcP5b activity was associated with density of TRAcP-positive osteoclasts in the subchondral bone of medial tibia plateaux. TRAcP-positive osteoclasts were more abundant in people with symptomatic knee osteoarthritis compared to controls. Serum TRAcP5b activity was associated with baseline pain and pain change.
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Although serum procollagen type-1 N-terminal propeptide (PINP) levels were not found to be different, tartrate-resistant acid phosphatase type 5b isoform (TRACP 5b) levels were significantly higher in the control group.
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Nidogen-2, a protein shown to be expressed intracellularly and for secretion by pre-adipocytes, was shown to interact, through its globular G3 domain, with TRAP 5a in vitro.
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Tartrate-resistant acid phosphatase deficiency in plasmacytoid dendritic cells leads to increased IFNalpha production, providing at least a partial explanation for how ACP5 mutations cause lupus in the context of spondyloenchondrodysplasia. Detection of ACP5 missense variants in a lupus cohort suggests that impaired tartrate-resistant acid phosphatase functioning may increase susceptibility to sporadic lupus
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Biallelic ACP5 mutations are associated with autoimmune cytopenias.
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Severe short stature can be the only presenting sign of ACP5 deficiency and the latter could therefore be considered as a rare cause in the differential diagnosis of severe, proportionate growth failure.
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Spondyloenchondrodysplasia (SPENCD) is a rare autosomal recessive skeletal dysplasia caused by recessive mutations in the ACP5 gene, and it is characterized by the persistence of chondroid tissue islands within the bone. [review]
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Data show that the levels of serum vascular endothelial growth factor (VEGF) and tartrate resistant acid phosphatase (TRacp-5b) are higher in multiple myeloma with cytogenetic abnormalities.
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A diverse spectrum of spondyloenchondrodysplasia phenotypes due to mutations in ACP5 has been presented.
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We identified five new biomarkers: GDF15, osteonectin, TRAP5, TWEAK, and YKL40 as being promising markers for monitoring bone metastases.
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Trap-5b is overexpressed in renal cell carcinoma patients with bone metastasis and bone resorption.
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Serum levels of NTx and TRACP5b are sensitive and simple biomarkers to indicate aberrant bone metabolism in giant cell tumor of bone, and they may have a clinical significance in GCT diagnosis.
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TRACP5a may be a promising chronic inflammatory marker and may play a prognostic role in cancer cachexia.
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TRACP5b has limited utility as a single marker of metabolic bone disease treatment.
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Immunohistochemistry revealed that ACP5 expression was positively correlated with FoxM1 expression in human HCC tissues, and their coexpression was associated with poor prognoses
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Pax6 binds endogenously to the proximal region of the tartrate acid phosphatase (TRAP) gene promoter and suppresses nuclear factor of activated T cells c1 (NFATc1)-induced TRAP gene expression.
