xCT Antibody - #DF12509
(143)
(63)
製品説明
ソース:
Rabbit
アプリケーション:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user. For optimal experimental results, antibody reuse is not recommended.
*Tips:
*The optimal dilutions should be determined by the end user. For optimal experimental results, antibody reuse is not recommended.
*Tips:
WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.
反応性:
Human,Mouse,Rat,Monkey
予測:
Pig(93%), Horse(93%), Rabbit(93%), Dog(93%)
クローナリティ:
Polyclonal
特異性:
xCT Antibody detects endogenous levels of total xCT.
RRID:
AB_2845314
引用形式: Affinity Biosciences Cat# DF12509, RRID:AB_2845314.
引用形式: Affinity Biosciences Cat# DF12509, RRID:AB_2845314.
コンジュゲート:
Unconjugated.
精製:
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.
別名:
折りたたみ／展開
Amino acid transport system xc xCT antibody; Amino acid transport system xc-; Calcium channel blocker resistance protein CCBR1; Calcium channel blocker resistance protein CCBR1 antibody; CCBR1; Cysteine/glutamate transporter antibody; Cystine/glutamate transporter; OTTHUMP00000164578; SLC7A11; Solute carrier family 7 (anionic amino acid transporter light chain, xc- system), member 11; solute carrier family 7; Solute carrier family 7 member 11; Solute carrier family 7, (cationic amino acid transporter, y+ system) member 11; SYSTEM Xc(-) TRANSPORTER-RELATED PROTEIN; xCT; XCT_HUMAN;
免疫原
免疫原:
A synthesized peptide derived from human xCT, corresponding to a region within the internal amino acids.
Uniprot:
遺伝子(ID):
タンパク質配列:
- Q9UPY5 XCT_HUMAN:
- Protein BLAST With
- NCBI/
- ExPASy/
- Uniprot
MVRKPVVSTISKGGYLQGNVNGRLPSLGNKEPPGQEKVQLKRKVTLLRGVSIIIGTIIGAGIFISPKGVLQNTGSVGMSLTIWTVCGVLSLFGALSYAELGTTIKKSGGHYTYILEVFGPLPAFVRVWVELLIIRPAATAVISLAFGRYILEPFFIQCEIPELAIKLITAVGITVVMVLNSMSVSWSARIQIFLTFCKLTAILIIIVPGVMQLIKGQTQNFKDAFSGRDSSITRLPLAFYYGMYAYAGWFYLNFVTEEVENPEKTIPLAICISMAIVTIGYVLTNVAYFTTINAEELLLSNAVAVTFSERLLGNFSLAVPIFVALSCFGSMNGGVFAVSRLFYVASREGHLPEILSMIHVRKHTPLPAVIVLHPLTMIMLFSGDLDSLLNFLSFARWLFIGLAVAGLIYLRYKCPDMHRPFKVPLFIPALFSFTCLFMVALSLYSDPFSTGIGFVITLTGVPAYYLFIIWDKKPRWFRIMSEKITRTLQIILEVVPEEDKL
種類予測
種類予測:
Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.
Species
Results
Score
Pig
93
Horse
93
Dog
93
Rabbit
93
Xenopus
79
Chicken
77
Zebrafish
64
Bovine
0
Sheep
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence
High(score>80) Medium(80>score>50) Low(score<50) No confidence
研究背景
機能:
Sodium-independent, high-affinity exchange of anionic amino acids with high specificity for anionic form of cystine and glutamate.
細胞の位置付け:
Membrane>Multi-pass membrane protein.
タンパク質ファミリー:
Belongs to the amino acid-polyamine-organocation (APC) superfamily. L-type amino acid transporter (LAT) (TC 2.A.3.8) family.
研究領域
· Cellular Processes > Cell growth and death > Ferroptosis. (View pathway)
参考文献
1). Exosomes secreted from cardiomyocytes suppress the sensitivity of tumor ferroptosis in ischemic heart failure. Signal transduction and targeted therapy, 2023
(PubMed: 36967385)
[IF=40.8]
2). NIR-responsive bio-system with sequential antibacterial and immunomodulatory effects for the treatment of periodontitis. Bioactive materials, 2025
(PubMed: 40496626)
[IF=18.9]
Application: WB Species: Rat Sample:
Fig. 5. Hemin@ER-IR808 promoted mitophagy of macrophages. (A) The TEM images of macrophages with different treatment, scale bar: 500 nm. (B) The protein expression of Nrf2, HO-1, SLC7A11, GPX4, PINK1 and Parkin2. (C) The semi-quantitative analysis of panel B. (D) The confocal images of JC-1 in macrophages, scale bar: 20 μm. (E) The semi-quantitative analysis of panel D. Groups setting: (1) Control group, macrophages without any treatment; (2) P. g group, macrophages with intracellular P. g infection; (4) NIR + Hemin@ER group, macrophages with intracellular P. g infection, Hemin@ER treatment and NIR irradiation; (5) NIR + Hemin@ER-IR808 group, macrophages with intracellular P. g infection, Hemin@ER-IR808 treatment and NIR irradiation. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001 (vs. (1) Control group); #P < 0.05, ##P < 0.01, ###P < 0.001 (vs. (2) P. g group); ⋇P < 0.05,⋇⋇P < 0.01, ⋇⋇⋇P < 0.001 (vs. (4) NIR + Hemin@ER group).
3). Polyamine-mediated ferroptosis amplification acts as a targetable vulnerability in cancer. Nature communications, 2024
(PubMed: 38504107)
[IF=16.6]
4). Targeting ALDH16A1 mediated thioredoxin lysosomal degradation to enhance ferroptosis susceptibility in SMARCA4-deficient NSCLC. Nature communications, 2025
(PubMed: 40897711)
[IF=16.6]
5). Piezo1 Upregulation in Monocyte-Derived Macrophages Impairs Post-Myocardial Infarction Cardiac Repair via Defective Efferocytosis and Enhanced Ferroptosis. Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025
(PubMed: 41214880)
[IF=15.1]
Application: WB Species: Mouse Sample:
Figure 5 Piezo1 induced defective efferocytosis in MoMs via SLC7A11 upregulation. A) Cluster analysis of the differentially expressed genes (|log2Fold Change| > 1, p < 0.05) identified by RNA-seq of BMDMs treated with DMSO or Yoda1 (5 µm) for 12 h) B. GO analysis revealed the enriched biological processes (BPs). C) The 17 genes upregulated according to the GO_BP analysis, including genes with read counts >1000, were analyzed by quantitative PCR in BMDMs from Piezo1fl/fl+MI and Piezo1Lyz2+MI mice (n = 6 mice per group). D. Quantitative PCR analysis of the 17 genes downregulated according to the GO_BP analysis, including genes with read counts >1000 (n = 6 mice per group). E) Representative Western blots and quantification showing SLC7A11 and SLC15A3 protein levels in BMDMs treated with DMSO or Yoda1 (5 µm) for 12 h (n = 4). F,G) Representative Western blots and quantification of SLC7A11, SLC15A3 and Piezo1 protein levels in BMDMs from Piezo1Lyz2+MI and Piezo1fl/fl+MI mice (n = 6 mice per group). H) Confocal microscopy images and quantification of BMDMs (F4/80, red) that engulfed PKH67-labeled apoptotic Jurkat cells (green) (n = 4). The data in (C, D, E and F) were analyzed by unpaired Student's t test. Other data were analyzed via one-way ANOVA, followed by the Bonferroni post hoc correction.
6). 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]
7). 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]
8). Carbon dots-mediated lysosomal iron sequestration for cancer immunostimulation. Chemical Engineering Journal, 2025
[IF=12.9]
9). PRODH2-Mediated Metabolism in the Bone Microenvironment Promotes Breast Cancer Metastasis. Cancer research, 2025
(PubMed: 40749014)
[IF=12.5]
Application: WB Species: Mouse Sample:
Figure 4. PRODH2 suppresses ferroptosis and regulates osteoclast differentiation. A, Untargeted metabolomics analysis in PRODH2-overexpressing cells vs. vector cells with treatment of Hyp. B, Changes in intracellular GSH levels upon PRODH2 overexpression (OE) or knockout in SCP2 cells with treatment of Hyp. C, Western blot analysis of ferroptosis-related proteins in indicated cells following Hyp treatment. Band intensities were normalized to β-actin and expressed as fold change relative to control. D, mRNA expression levels of SLC7A11 in different PRODH2 expression conditions with treatment of Hyp. E, Relative expression levels of intracellular GSH in breast cancer indicated cells with treatment of Hyp. F, Representative images and quantitative analysis of C11-BODIPY oxidation (green)/reduction (red) ratio in cells. Scale bar, 100 μm. G, Representative staining images and quantification of osteoclast differentiation in the presence of CM from indicated cells with treatment of Hyp. Black arrows, multinuclear TRAP+ osteoclasts. Scale bar, 100 μm. H, Left, μCT, hematoxylin and eosin (H&E), and TRAP staining images of bone metastasis in mice after intracardiac injection. Right, quantification of the positive area of Sirius red staining, BLI signals, μCT osteolytic lesion sites, and TRAP+ osteoclasts along the bone–tumor interface of metastases. n = 6 mice per group. Each experiment was performed in triplicate and independently repeated three times. Data are presented as the mean ± SD of n = 3 biologically independent samples. Scale bar, 100 μm. *, P < 0.05; **, P < 0.01. B, bone, T, tumor; M, marrow; NC, negative control.
Application: IF/ICC Species: Mouse Sample:
Figure 4. PRODH2 suppresses ferroptosis and regulates osteoclast differentiation. A, Untargeted metabolomics analysis in PRODH2-overexpressing cells vs. vector cells with treatment of Hyp. B, Changes in intracellular GSH levels upon PRODH2 overexpression (OE) or knockout in SCP2 cells with treatment of Hyp. C, Western blot analysis of ferroptosis-related proteins in indicated cells following Hyp treatment. Band intensities were normalized to β-actin and expressed as fold change relative to control. D, mRNA expression levels of SLC7A11 in different PRODH2 expression conditions with treatment of Hyp. E, Relative expression levels of intracellular GSH in breast cancer indicated cells with treatment of Hyp. F, Representative images and quantitative analysis of C11-BODIPY oxidation (green)/reduction (red) ratio in cells. Scale bar, 100 μm. G, Representative staining images and quantification of osteoclast differentiation in the presence of CM from indicated cells with treatment of Hyp. Black arrows, multinuclear TRAP+ osteoclasts. Scale bar, 100 μm. H, Left, μCT, hematoxylin and eosin (H&E), and TRAP staining images of bone metastasis in mice after intracardiac injection. Right, quantification of the positive area of Sirius red staining, BLI signals, μCT osteolytic lesion sites, and TRAP+ osteoclasts along the bone–tumor interface of metastases. n = 6 mice per group. Each experiment was performed in triplicate and independently repeated three times. Data are presented as the mean ± SD of n = 3 biologically independent samples. Scale bar, 100 μm. *, P < 0.05; **, P < 0.01. B, bone, T, tumor; M, marrow; NC, negative control.
Application: IHC Species: Mouse Sample:
Figure 4. PRODH2 suppresses ferroptosis and regulates osteoclast differentiation. A, Untargeted metabolomics analysis in PRODH2-overexpressing cells vs. vector cells with treatment of Hyp. B, Changes in intracellular GSH levels upon PRODH2 overexpression (OE) or knockout in SCP2 cells with treatment of Hyp. C, Western blot analysis of ferroptosis-related proteins in indicated cells following Hyp treatment. Band intensities were normalized to β-actin and expressed as fold change relative to control. D, mRNA expression levels of SLC7A11 in different PRODH2 expression conditions with treatment of Hyp. E, Relative expression levels of intracellular GSH in breast cancer indicated cells with treatment of Hyp. F, Representative images and quantitative analysis of C11-BODIPY oxidation (green)/reduction (red) ratio in cells. Scale bar, 100 μm. G, Representative staining images and quantification of osteoclast differentiation in the presence of CM from indicated cells with treatment of Hyp. Black arrows, multinuclear TRAP+ osteoclasts. Scale bar, 100 μm. H, Left, μCT, hematoxylin and eosin (H&E), and TRAP staining images of bone metastasis in mice after intracardiac injection. Right, quantification of the positive area of Sirius red staining, BLI signals, μCT osteolytic lesion sites, and TRAP+ osteoclasts along the bone–tumor interface of metastases. n = 6 mice per group. Each experiment was performed in triplicate and independently repeated three times. Data are presented as the mean ± SD of n = 3 biologically independent samples. Scale bar, 100 μm. *, P < 0.05; **, P < 0.01. B, bone, T, tumor; M, marrow; NC, negative control.
10). Retinol Saturase Mediates Retinoid Metabolism to Impair a Ferroptosis Defense System in Cancer Cells. Cancer research, 2023
(PubMed: 37184371)
[IF=12.5]
Restrictive clause
Affinity Biosciences tests all products strictly. Citations are provided as a resource for additional applications that have not been validated by Affinity Biosciences. Please choose the appropriate format for each application and consult Materials and Methods sections for additional details about the use of any product in these publications.
For Research Use Only.
Not for use in diagnostic or therapeutic procedures. Not for resale. Not for distribution without written consent. Affinity Biosciences will not be held responsible for patent infringement or other violations that may occur with the use of our products. Affinity Biosciences, Affinity Biosciences Logo and all other trademarks are the property of Affinity Biosciences LTD.