产品: NCOA4 抗体
货号: DF4255
描述: Rabbit polyclonal antibody to NCOA4
应用: WB IHC IF/ICC
文献验证: WB, IF/ICC
反应: Human, Mouse, Rat
分子量: 70~90KD; 70kD(Calculated).
蛋白号: Q13772
RRID: AB_2836606

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产品描述

来源:
Rabbit
应用:
WB 1:500-1:1000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

反应:
Human, Mouse, Rat
克隆:
Polyclonal
特异性:
NCOA4 Antibody detects endogenous levels of total NCOA4.
RRID:
AB_2836606
引用格式: Affinity Biosciences Cat# DF4255, RRID:AB_2836606.
偶联:
Unconjugated. 130
纯化:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
保存:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
别名:

展开/折叠

70 kDa androgen receptor activator; 70 kDa androgen receptor coactivator; 70 kDa AR activator; 70 kDa AR-activator; Androgen receptor coactivator 70 kD; Androgen receptor coactivator 70 kDa protein; Androgen receptor-associated protein of 70 kDa; ARA 70; ARA70; DKFZp762E1112; ELE 1; ELE1; ELE1/ret TK; NCOA 4; NCoA-4; NCOA4; NCOA4_HUMAN; Nuclear receptor coactivator 4; Papillary thyroid carcinoma 3; PTC 3; PTC3; RET activating gene ELE1; Ret activating protein ELE1; Ret-activating protein ELE1; RFG;

抗原和靶标

免疫原:
Uniprot:
基因/基因ID:
表达:
Q13772 NCOA4_HUMAN:

Widely expressed. Also detected in adipose tissues and in different cell lines. Isoform Beta is only expressed in testis.

序列:
MNTFQDQSGSSSNREPLLRCSDARRDLELAIGGVLRAEQQIKDNLREVKAQIHSCISRHLECLRSREVWLYEQVDLIYQLKEETLQQQAQQLYSLLGQFNCLTHQLECTQNKDLANQVSVCLERLGSLTLKPEDSTVLLFEADTITLRQTITTFGSLKTIQIPEHLMAHASSANIGPFLEKRGCISMPEQKSASGIVAVPFSEWLLGSKPASGYQAPYIPSTDPQDWLTQKQTLENSQTSSRACNFFNNVGGNLKGLENWLLKSEKSSYQKCNSHSTTSSFSIEMEKVGDQELPDQDEMDLSDWLVTPQESHKLRKPENGSRETSEKFKLLFQSYNVNDWLVKTDSCTNCQGNQPKGVEIENLGNLKCLNDHLEAKKPLSTPSMVTEDWLVQNHQDPCKVEEVCRANEPCTSFAECVCDENCEKEALYKWLLKKEGKDKNGMPVEPKPEPEKHKDSLNMWLCPRKEVIEQTKAPKAMTPSRIADSFQVIKNSPLSEWLIRPPYKEGSPKEVPGTEDRAGKQKFKSPMNTSWCSFNTADWVLPGKKMGNLSQLSSGEDKWLLRKKAQEVLLNSPLQEEHNFPPDHYGLPAVCDLFACMQLKVDKEKWLYRTPLQM

研究背景

功能:

Enhances the androgen receptor transcriptional activity in prostate cancer cells. Ligand-independent coactivator of the peroxisome proliferator-activated receptor (PPAR) gamma.

组织特异性:

Widely expressed. Also detected in adipose tissues and in different cell lines. Isoform Beta is only expressed in testis.

亚基结构:

Interacts with the androgen receptor and the retinoid X receptor (RXR) in a ligand-dependent manner.

研究领域

· Cellular Processes > Cell growth and death > Ferroptosis.   (View pathway)

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Thyroid cancer.   (View pathway)

文献引用

1). FOXO1-NCOA4 Axis Contributes to Cisplatin-Induced Cochlea Spiral Ganglion Neuron Ferroptosis via Ferritinophagy. Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024 (PubMed: 39206719) [IF=15.1]

2). Metabolomic and Cellular Mechanisms of Drug-Induced Ototoxicity and Nephrotoxicity: Therapeutic Implications of Uric Acid Modulation. Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025 (PubMed: 40041973) [IF=15.1]

3). Internalized polystyrene nanoplastics trigger testicular damage and promote ferroptosis via CISD1 downregulation in mouse spermatocyte. JOURNAL OF NANOBIOTECHNOLOGY, 2025 [IF=12.6]

Application: IF/ICC    Species: Mouse    Sample: GC-2 cells

Fig. 5 3-MA and NCOA4 knockdown suppress PS-NPs-induced ferritinophagy. (A) GO analysis based on proteomic analysis results of PS-NPs-treated group and control group. (B and C) Heat maps of ferroptosis-related and autophagy-related proteins in vehicle and PS-NPs-treated GC-2 cells. (D) Immunofluorescence of LC3 in GC-2 cells treated with PS-NPs. (E) Relative expression of ferritinophagy-related gene in GC-2 cells post-treatment PS-NPs. (F and G) Ferritinophagy-related protein expression in PS-NPs-stimulated GC-2 cells. (H) Immunofluorescence of NCOA4 and FTH1 in GC-2 cells treated with PS-NPs. Line intensity plots show colocalization between FTH1 (red) and NCOA4 (green). (I) The cell viability was assayed in GC-2 cells following PS-NPs treatment with or without 3-MA. (J) Immunofluorescence staining of LC3 in GC-2 cells post-treatment with PS-NPs and 3-MA. (K and L) Western blotting and quantitative analysis of NCOA4 and FTH1. (M) Immunofluorescence of NCOA4 and FTH1 in GC-2 cells following PS-NPs and 3-MA treatment. Line intensity plots show colocalization between FTH1 (red) and NCOA4 (green). (N) The viability of PS-NPs-stimulated GC-2 cells while simultaneously inhibiting NCOA4 expression. (O and P) Representative fluorescent images and quantitative analysis of lipid peroxidation levels in PS-NPs-stimulated GC-2 cells while simultaneously inhibiting NCOA4 expression. (Q and R) Intracellular chelatable iron in GC-2 cells after 12 h exposure to PS-NPs while inhibiting NCOA4 expression stained with FerroOrange. (S and T) Representative fluorescent images and quantification of ROS levels using the fluorescent indicator DCFH-DA in GC-2 cells after 12 h exposure to PS-NPs while inhibiting NCOA4 expression

Application: WB    Species: Mouse    Sample: GC-2 cells

Fig. 5 3-MA and NCOA4 knockdown suppress PS-NPs-induced ferritinophagy. (A) GO analysis based on proteomic analysis results of PS-NPs-treated group and control group. (B and C) Heat maps of ferroptosis-related and autophagy-related proteins in vehicle and PS-NPs-treated GC-2 cells. (D) Immunofluorescence of LC3 in GC-2 cells treated with PS-NPs. (E) Relative expression of ferritinophagy-related gene in GC-2 cells post-treatment PS-NPs. (F and G) Ferritinophagy-related protein expression in PS-NPs-stimulated GC-2 cells. (H) Immunofluorescence of NCOA4 and FTH1 in GC-2 cells treated with PS-NPs. Line intensity plots show colocalization between FTH1 (red) and NCOA4 (green). (I) The cell viability was assayed in GC-2 cells following PS-NPs treatment with or without 3-MA. (J) Immunofluorescence staining of LC3 in GC-2 cells post-treatment with PS-NPs and 3-MA. (K and L) Western blotting and quantitative analysis of NCOA4 and FTH1. (M) Immunofluorescence of NCOA4 and FTH1 in GC-2 cells following PS-NPs and 3-MA treatment. Line intensity plots show colocalization between FTH1 (red) and NCOA4 (green). (N) The viability of PS-NPs-stimulated GC-2 cells while simultaneously inhibiting NCOA4 expression. (O and P) Representative fluorescent images and quantitative analysis of lipid peroxidation levels in PS-NPs-stimulated GC-2 cells while simultaneously inhibiting NCOA4 expression. (Q and R) Intracellular chelatable iron in GC-2 cells after 12 h exposure to PS-NPs while inhibiting NCOA4 expression stained with FerroOrange. (S and T) Representative fluorescent images and quantification of ROS levels using the fluorescent indicator DCFH-DA in GC-2 cells after 12 h exposure to PS-NPs while inhibiting NCOA4 expression

4). Arsenic induces pancreatic dysfunction and ferroptosis via mitochondrial ROS-autophagy-lysosomal pathway. JOURNAL OF HAZARDOUS MATERIALS, 2020 (PubMed: 31735470) [IF=12.2]

Application: WB    Species: Rat    Sample: MIN6 cells

Fig. 6 Ferroptosis was triggered by MtROS-dependent autophagy. (A) Effects of NaAsO2 (4  and TEMPO on LC3 and p62 in MIN6 cells. (B) Autophagic flux analysis. (C) The efficiency of CQ, and its effect on GPX4 and COX-2 in NaAsO2- Journal Pre-proof treated MIN6 cells. (D) Effects of NaAsO2 and CQ on relative GSH, T-SOD, and MDA content in MIN6 cells. (E) Effects of CQ on the NaAsO2-induced accumulation of lipid ROS by BODIPY 581/591 C11 staining (scale bar = 50 m). (F) Effects of CQ on the NaAsO2-induced insulin released using an ELISA kit. All results are expressed as the mean ± SD, n = 3. *P < 0.05, **P < 0.001 vs. control group, #P < 0.05, ##P < 0.001 vs. NaAsO2 group.

5). Liraglutide and GLP-1(9-37) alleviated hepatic ischemia-reperfusion injury by inhibiting ferroptosis via GSK3β/Nrf2 pathway and SMAD159/Hepcidin/FTH pathway. Redox biology, 2024 (PubMed: 39693850) [IF=11.4]

6). Induction of autophagy via the ROS-dependent AMPK-mTOR pathway protects copper-induced spermatogenesis disorder. Redox Biology, 2022 (PubMed: 34979450) [IF=10.7]

Application: WB    Species: Mouse    Sample: GC-1 spg cells

Fig. 8 Autophagy triggered ferroptosis in CuSO4-treated GC-1 spg cells. (a) Cells were treated with CuSO4 (0, 0.4, 0.8 and 1.6 mM) for 12h and 24h. The Western blot results of GPX4 and COX-2 protein expression. (b) The quantification of GPX4 and COX-2. (c) Cells were treated with CuSO4 (1.6 mM, 24h) in the presence/absence of 3-MA (1 mM, 1h), the changes of GPX4, COX-2, NCOA4 and FTH1. (d) Cells transfected with control shRNA and ATG5 shRNA exposed with CuSO4 (1.6 mM) for 24 h, changes of GPX4, COX-2, NCOA4 and FTH1. Data are presented with the means ± standard deviation. *p < 0.05 **p < 0.01.

7). ZnO NPs induce miR-342-5p mediated ferroptosis of spermatocytes through the NF-κB pathway in mice. Journal of nanobiotechnology, 2024 (PubMed: 38961442) [IF=10.2]

8). ZnO NPs induce miR-342-5p mediated ferroptosis of spermatocytes through the NF-κB pathway in mice. Journal of nanobiotechnology, 2024 (PubMed: 38961442) [IF=10.2]

Application: WB    Species: Mouse    Sample: GC-2 cells

Fig. 6 ZnO NPs induce the ferroptosis of GC-2 cells. (A) Intracellular chelatable iron in GC-2 cells treated with or without ZnO NPs stained with PGSK (green). Statistical analysis of MFI of PGSK was shown. (B) Representative FACS data for lipid peroxidation level in GC-2 cells following ZnO NPs treatment using C11 BODIPY. Statistical analysis of MFI of the ratio of green/red was shown. (C) qRT-PCR analysis of ferroptosis-related gene expression in GC-2 cells after ZnO NPs treatment. (D) Western blot of ferroptosis-related protein levels in GC-2 cells treated with ZnO NPs. Statistical analysis of mean grey values ratios of the corresponding proteins/β-actin was shown, the same as below. (E) The cell viability of GC-2 cells following ZnO NPs treatment with or without Fer-1 (3.5 µM). (F) Intracellular chelatable iron in GC-2 cells following ZnO NPs treatment with or without Fer-1 stained with PGSK. Statistical analysis of MFI of PGSK was shown. (G) Representative FACS data of lipid peroxidation level in GC-2 cells following ZnO NPs treatment with or without Fer-1 stained with C11 BODIPY. Statistical analysis of MFI of the ratio of green/red was shown. (H and I) The levels of GSH and MDA in GC-2 cells following ZnO NPs treatment with or without Fer-1. (J) qRT-PCR analysis of ferroptosis-related gene expression in GC-2 cells following ZnO NPs treatment with or without Fer-1. (K) Western blot of ferroptosis-related protein levels in GC-2 cells following ZnO NPs treatment with or without Fer-1

9). Defective ferritinophagy and imbalanced iron metabolism in PBDE-47-triggered neuronal ferroptosis and salvage by Canolol. The Science of the total environment, 2024 (PubMed: 38750757) [IF=8.2]

10). STING promotes ferroptosis through NCOA4-dependent ferritinophagy in acute kidney injury. Free radical biology & medicine, 2023 (PubMed: 37634745) [IF=7.1]

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