cxcl10 protein level (Elabscience Biotechnology)
Structured Review

Cxcl10 Protein Level, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cxcl10+protein+level/pmc09091994-44-0-16?v=Elabscience+Biotechnology
Average 90 stars, based on 2 article reviews
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1) Product Images from "CXCL10 is a novel anti‐angiogenic factor downstream of p53 in cardiomyocytes"
Article Title: CXCL10 is a novel anti‐angiogenic factor downstream of p53 in cardiomyocytes
Journal: Physiological Reports
doi: 10.14814/phy2.15304
Figure Legend Snippet: p53 induced CXCL10 expression in cardiomyocytes. DNA microarray was performed using p53‐overexpressing NRCMs. (a) Scatter plot shows the genes colored blue with >2‐fold upregulate in p53‐overexpressing NRCMs compared with β‐gal. (b) Heat map shows genes colored red with >2‐fold change and green with <0.5‐fold change between β‐gal and p53. (c) Gene ontology analysis. (d, e) The expression of (d) CXCL10 and (e) p21 transcripts was measured by qPCR ( n = 4). Experiments were performed three times with similar results. (f) The protein expression of CXCL10 in culture media of p53‐overexpressing NRCMs was measured by ELISA ( n = 3). * p < 0.05, ** p < 0.01. by Student's t ‐test.
Techniques Used: Expressing, Microarray, Enzyme-linked Immunosorbent Assay
Figure Legend Snippet: Doxorubicin induced the expression of CXCL10 in cardiomyocytes through p53 in cardiomyocytes. (a–h) NRCMs were stimulated with Doxo for indicated concentration and time. (i–l) NRCMs were transfected with siRNA for p53 (sip53) or control (siCon) for 48 h, followed by stimulation with Doxo for 24 h. The expression of p53 (a, e, i) and CXCL10 (b, f, j) mRNA was measured by qPCR. ( n = 3). (c, g, k) The expression of p53 protein was analyzed by immunoblotting. Representative data are shown. (d, h, l) The band intensities of p53 were measured ( n = 3). Experiments were performed three times with similar results. (a–h). *p < 0.05, **p < 0.01 by one‐way ANOVA followed by Dunnett test. (i–l) * p < 0.05, ** p < 0.01 by one‐way ANOVA followed by Tukey–Kramer test.
Techniques Used: Expressing, Concentration Assay, Transfection, Control, Western Blot
Figure Legend Snippet: Hypoxia synergistically elevated the expression of CXCL10. p53‐overexpresisng NRCMs were treated with CoCl2 for 24 h. (a) The expression of p53 and GAPDH protein was analyzed by immunoblotting. Representative data were shown. The expression of (b) VEGF and (c) CXCL10 transcripts was measured by qPCR ( n = 4). Experiments were performed three times with similar results. * p < 0.05, ** p < 0.01 by one‐way ANOVA followed by Tukey–Kramer test.
Techniques Used: Expressing, Western Blot
Figure Legend Snippet: p53‐induced CXCL10, secreted from cardiomyocytes, inhibited the tube formation of endothelial cells. Culture media were collected from p53‐ or β‐gal‐overexpressing NRCMs. RAOECs were cultured with the conditioned media in the presence of AMG487, an inhibitor of CXCR3. Angiogenesis assay was performed. (a) Representative images were shown. (b) The number of tube formation was measured ( n = 6). * p < 0.05, ** p < 0.01 by one‐way ANOVA followed by Tukey–Kramer test.
Techniques Used: Cell Culture, Angiogenesis Assay
![XMT-2056 elicits potent antigen-dependent and Fc-R–mediated activation of monocytes in cocultures. A, Schematic of the XMT-2056 mechanism, which includes HER2-dependent ADC uptake into tumor cells and Fcγ-R–expressing myeloid cells. B, Chemical structure of XMT-2056. C, Cytokine induction as measured by a multiplex Luminex assay from supernatants of fresh human WBCs treated for 6 (IFN-β) or 24 <t>(CXCL10,</t> IL-6, and TNF-a) hours. Bars represent mean value of n = 2 data points shown as symbols. D, Competition with trastuzumab by biolayer interferometry (Octet): trastuzumab was loaded onto the sensor chip, and HER2 ECD or HT19 antibody associations are indicated by blue arrows. Additional binding by HT19 indicates noncompetitive binding. E, Competition with trastuzumab by cell-based flow cytometry. HT19 hIgG1 or mIgG2a formats detected with either Alexa Fluor anti-hIgG1 (h647) or Alexa Fluor anti-mIgG2a (m647) secondary antibodies in the presence or absence of trastuzumab–mIgG2a. Each point represents the mean and SD ( n = 3). F, Binding of XMT-2056 or HT19 antibody to HCC1954 cells showing fluorescence intensities measured by flow cytometry. Each point represents the mean and SD ( n = 2). G, CXCL10 cytokine induction in HCC1954 monocultures treated for 24 hours with XMT-2056, nonbinding control ADC, HT19, or the free payload. Each point represents the mean and SD ( n = 2). H, Binding of XMT-2056 or Fc-mutant XMT-2056, HT19, and nonbinding control ADC to SKOV3 cells showing fluorescence intensities measured by flow cytometry. Each point represents the mean and SD ( n = 3). I and J, IRF3 reporter activity of THP1 cells in coculture with SKOV3 cells ( I ) or cultured on recombinant HER2 antigen-coated plates ( J ) treated for 24 hours with XMT-2056 or Fc-mutant XMT-2056, nonbinding control ADC, or STING agonist payload. Each point represents the mean and SD ( n = 3). When noted, EC 50 and B max values represent mean of two independent experiments. gMFI, geometric mean fluorescence intensity; RLU, relative light units. ( A, Created in BioRender. Cetinbas, N. [2025], https://BioRender.com/s16c825 ; G, Created in BioRender. Cetinbas, N. [2025], https://BioRender.com/s16c825 ; I and J, Created in BioRender. Cetinbas, N. [2025], https://BioRender.com/s16c825 .)](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_0966/pmc12010966/pmc12010966__ccr-24-2449_f1.jpg)

