Rat ACP5 ELISA
- Known as:
- Rat ACP5 Enzyme-linked immunosorbent assay test
- Catalog number:
- kt-5381
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- Rat ACP5 ELISA
Related genes to: Rat ACP5 ELISA
- Gene:
- ACP5 NIH gene
- Name:
- acid phosphatase 5, tartrate resistant
- Previous symbol:
- -
- Synonyms:
- TRAP, HPAP
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1989-02-23
- Date modifiied:
- 2019-04-23
Related products to: Rat ACP5 ELISA
Related articles to: Rat ACP5 ELISA
- The major goal of this study was to compare mRNA expression associated with water homeostasis in intestines of high water efficient (HWE) broilers to expression in unselected Modern Random Bred (MRB) broilers under thermoneutral (TN) and heat stress (HS) environments. - Source: PubMed
Publication date: 2026/05/13
Lassiter KentuAloui LoujainGreene Elizabeth SMaqaeda MarcielaSchaeffer KirstenRoach BrookleeTabler TravisWideman Robert FOrlowski SaraDridi SamiBottje Walter G - Bone metastases (BMs) of non-small cell lung cancer (NSCLC) are associated with skeletal-related events that impair quality of life. Tartrate-resistant acid phosphatase 5b (TRACP-5b) is considered a marker of osteoclastic activity; however, its prognostic utility for NSCLC patients with BMs remains unclear. This study aimed to evaluate the association between longitudinal changes in TRACP-5b and BM progression in a relatively homogeneous population of patients with epidermal growth factor receptor (EGFR)-mutated NSCLC treated with osimertinib. - Source: PubMed
Ikegami KeisukeMakihara Reiko AndoShinno YukiTateishi AkikoMizutani TomonoriOkuma YusukeYoshida TatsuyaHorinouchi HidehitoYamamoto NoboruHashimoto HironobuHori SatokoGoto Yasushi - Excessive bone resorption by osteoclasts causes pathological bone loss in diseases such as osteoporosis. 7-Deacetoxy-7-oxogedunin (CG-1), a limonoid isolated from (Meliaceae), exhibits various biological activities. Here, we examined the anti-osteoclastogenic effect of CG-1 and its underlying mechanism in receptor activator of NF-κB ligand (RANKL)-induced osteoclast differentiation of RAW264.7 cells. CG-1 inhibited the formation of tartrate-resistant acid phosphatase-positive multinucleated cells and decreased the expression of osteoclastogenesis-related genes. When CG-1 was added to the culture during the first 3 days of the 5-day-osteoclastogenesis period, the expression levels of the osteoclastogenesis-related genes (, , , , and ) were decreased, as was observed when CG-1 was added continuously for 5 days. Furthermore, CG-1 lowered RANKL-induced Akt phosphorylation, which is similar to the results seen with the PI3K inhibitor, LY294002. Moreover, CG-1 and LY294002 suppressed the RANKL-induced expression of NFATc1, the master transcription factor for regulating terminal differentiation into osteoclasts. These results suggest that CG-1 attenuated RANKL-induced osteoclastogenesis by inhibiting the PI3K/Akt-NFATc1 axis during the early stage of osteoclast differentiation. Thus, CG-1 has the potential to suppress osteoclast-mediated bone resorption. - Source: PubMed
Publication date: 2026/05/07
Koike AtsushiFujimori Ko - Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease characterized by persistent synovial inflammation and progressive joint destruction. Numerous clinical studies have revealed that exercise is extremely beneficial for the outcome of RA. However, the underlying mechanism remains poorly understood. In the present study, we investigated the therapeutic efficacy of irisin, an exercise hormone, on K/BxN serum and collagen-induced arthritis (CIA), two well established mouse models for RA research. Mechanistically, irisin interacted with ITGAV (integrin subunit alpha V) and ITGB5 (integrin subunit beta 5) to activate mitophagy and remove leaked mitochondrial DNA (mtDNA) and reactive oxygen species (ROS), which suppressed the activation of NLRP3 (NLR family pyrin domain containing 3) inflammasome and then hindered the pathological process of experimental arthritis. Notably, the beneficial effects of irisin on the treatment of experimental arthritis were significantly abolished in mice with (autophagy related 5) conditional knockout in myeloid cells (). Our study elucidated the underlying mechanism through which exercise alleviated experimental arthritis and offered a feasible therapeutic strategy for RA. 3-MA: 3-methyladenine Ac-TUBA: acetylated TUBA; ACP5: acid phosphatase 5, tartrate resistant; AIM2: absent in melanoma 2; ANOVA: analysis of variance; ATP: adenosine triphosphate; BAF: bafilomycin A; BV:TV: bone volume per total volume; BMD: bone mineral density; BMDMs: bone marrow-derived macrophages; CASP1: caspase 1; CTSB: cathepsin B; CIA: collagen-indcued arthritis; DNM1L: dynamin 1 like; CYCS: cytochrome c, somatic; EtBr: ethidium bromide; FNDC5: fibronectin type III domain containing 5; FL-GSDMD: GSDMD full length; GSDMD: gasdermin D; HE: hematoxylin and eosin; iBMDMs: immortalized bone marrow-derived macrophages; IL1B: interleukin 1 beta; IL6: interleukin 6; IL18: interleukin 18; LDH: lactate dehydrogenase; LPS: lipopolysaccharide; MAP1LC3: microtubule associated protein 1 light chain 3; MSU: monosodium urate; mtROS: mitochondrial reactive oxygen species; mtDNA: mitochondrial DNA; NLRC4: NLR family CARD domain containing 4; NLRP1: NLR family pyrin domain containing 1; NLRP3: NLR family pyrin domain containing 3; NT-GSDMD: GSDMD N-terminal fragment; NAC: N-acetylcysteine; ox-mtDNA: oxidized mitochondrial DNA; PYCARD: PYD and CARD domain containing; PRKAA: protein kinase AMP-activated catalytic subunit alpha 1; PINK1: PTEN induced kinase 1; PRKN: parkin RBR E3 ubiquitin protein ligase; RA: rheumatoid arthritis; ROS: reactive oxygen species; SD: standard deviation; SiO: silicon dioxide; SQSTM1: sequestosome 1; Tb.Th: trabecular thickness; Tb.N: trabecular number; Tp.Sp: trabecular separation; TNF/TNF-α: tumor necrosis factor; TOMM20: translocase of outer mitochondrial membrane 20; TUBA: tubulin alpha; ULK1: unc-51 like autophagy activating kinase 1; WT: wild type. - Source: PubMed
Publication date: 2026/06/01
Wu YanglinFu TingtingTeng YunPan YingLi LijunFeng YuLin Jun - Rheumatoidarthritis (RA) is an autoimmune disease accompanied by joint swelling,stiffness, and pain, leading to a sharp decline in quality of life. However,the treatment of RA still faces numerous challenges. Clinical studies indicatethat specific hypoglycemic agents alleviate the symptoms of RA, while the potentialmolecular mechanism remains unknown. Herein, we initially assess the efficacyof various categories of anti-diabetic medications including biguanides, GLP1R(glucagon like peptide 1 receptor) agonists, SLC5A2/SGLT2 (solute carrierfamily 5 member 2) inhibitors, DPP4 (dipeptidyl peptidase 4) inhibitors,sulfonylureas, thiazolidinediones, and insulin analog in RA models ofcollagen-induced arthritis (CIA) and serum-transfer arthritis (STA). Resultsdemonstrate that solely thiazolidinediones (pioglitazone [PIOG]) confersuperior efficacy, whereas the other anti-diabetic agents provide minimal or notherapeutic benefits. Mechanistically, thiazolidinediones (PIOG) activatesPPARG/PPARγ (peroxisome proliferator activated receptor gamma) to promotemitophagic flux, thereby inhibiting aberrant NLRP3 inflammasome activation andreducing pro-inflammatory factors IL1B/IL1-BETA (interleukin 1 beta) and IL18 (interleukin18) release. Notably, loss of autophagy either genetically or pharmacologicallysubstantially diminishes the anti-inflammatory effects of PIOG both in vitroand in vivo. In summary, these results offer new mechanistic insight intodisease crosstalk and support the translational value of thiazolidinedionesPIOG as a candidate for precision therapy in RA or multimorbidity of RA and type2 diabetes mellitus (T2DM). 3-MA: 3-methyladenine; ACP5/TRAP: acid phosphatase 5, tartrate resistant; AIM2: absent in melanoma 2; ALUM: aluminum hydroxide adjuvant; ANOVA: analysis of variance; PYCARD/ASC: PYD and CARD domain containing; ATP: adenosine triphosphate; BMDM: bone marrow-derived macrophage; BV:TV: bone volume:tissue volume; CIA: collagen-induced arthritis; DAPI: 4',6-diamidino-2-phenylindole; DNA: deoxyribonucleic acid; ELISA: enzyme-linked immunosorbent assay; FG: Fast Green; GFP: green fluorescent protein; GSDMD: gasdermin D; IL1B/IL1-BETA: interleukin 1 beta; IL18: interleukin 18; LDH: lactate dehydrogenase; LPS: lipopolysaccharide; Micro-CT: micro-computed tomography; MSU: monosodium urate; mtDNA: mitochondrial DNA; mtROS: mitochondrial reactive oxygen species; NAC: N-acetylcysteine; NLRP1B: NLR family, pyrin domain containing 1B; NLRP3: NLR family, pyrin domain containing 3; NLRC4: NLR family, CARD domain containing 4; OGTT: oral glucose tolerance test; PBS: phosphate-buffered saline; PINK1: PTEN induced putative kinase 1; PIOG: pioglitazone; PPARG/PPARγ: peroxisome proliferator activated receptor gamma; RA: rheumatoid arthritis; ROS: reactive oxygen species; STA: serum transfer arthritis; STZ: streptozotocin; T2DM: type 2 diabetes mellitus; Tb.N: trabecular number; Tb.Sp: trabecular separation; Tb.Th: trabecular thickness; THP-1: human monocytic leukemia cell line; TNF/TNF-α: tumor necrosis factor; TOMM20: translocase of outer mitochondrial membrane 20. - Source: PubMed
Publication date: 2026/05/25
Fu TingtingWu YanglinWang BoZhang QinGuo LujunHan ZezhangCao JiaLin Jun