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ABclonal Biotechnology
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ABclonal Biotechnology
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Image Search Results
Journal: iScience
Article Title: Postnatal expression of cell cycle promoter Fam64a causes heart dysfunction by inhibiting cardiomyocyte differentiation through repression of Klf15
doi: 10.1016/j.isci.2022.104337
Figure Lengend Snippet:
Article Snippet: Primary antibodies used were for Klf15 (NBP2-24635, Novus Biologicals, USA), Trim28 (#4124, Cell Signaling Technology, USA), GR (sc-393232, Santa Cruz Biotechnology, USA), Myh7 (A4963, ABclonal, USA), Nppa (A14755, ABclonal), Tnnt1 (A10354, ABclonal), Acta2 (A7248, ABclonal), Myl4 (A13249, ABclonal), Arntl (A17334, ABclonal),
Techniques: Expressing, Recombinant, Plasmid Preparation, Luciferase, RNA Sequencing Assay, Sequencing, Software
Journal: iScience
Article Title: Postnatal expression of cell cycle promoter Fam64a causes heart dysfunction by inhibiting cardiomyocyte differentiation through repression of Klf15
doi: 10.1016/j.isci.2022.104337
Figure Lengend Snippet:
Article Snippet: Primary antibodies used were for Klf15 (NBP2-24635, Novus Biologicals, USA), Trim28 (#4124, Cell Signaling Technology, USA), GR (sc-393232, Santa Cruz Biotechnology, USA), Myh7 (A4963, ABclonal, USA), Nppa (A14755, ABclonal), Tnnt1 (A10354, ABclonal), Acta2 (A7248, ABclonal),
Techniques: Expressing, Recombinant, Plasmid Preparation, Luciferase, RNA Sequencing Assay, Sequencing, Software
Journal: iScience
Article Title: Postnatal expression of cell cycle promoter Fam64a causes heart dysfunction by inhibiting cardiomyocyte differentiation through repression of Klf15
doi: 10.1016/j.isci.2022.104337
Figure Lengend Snippet:
Article Snippet: Primary antibodies used were for Klf15 (NBP2-24635, Novus Biologicals, USA), Trim28 (#4124, Cell Signaling Technology, USA), GR (sc-393232, Santa Cruz Biotechnology, USA), Myh7 (A4963, ABclonal, USA), Nppa (A14755, ABclonal),
Techniques: Expressing, Recombinant, Plasmid Preparation, Luciferase, RNA Sequencing Assay, Sequencing, Software
Journal: iScience
Article Title: Postnatal expression of cell cycle promoter Fam64a causes heart dysfunction by inhibiting cardiomyocyte differentiation through repression of Klf15
doi: 10.1016/j.isci.2022.104337
Figure Lengend Snippet:
Article Snippet: Primary antibodies used were for Klf15 (NBP2-24635, Novus Biologicals, USA), Trim28 (#4124, Cell Signaling Technology, USA), GR (sc-393232, Santa Cruz Biotechnology, USA), Myh7 (A4963, ABclonal, USA), Nppa (A14755, ABclonal), Tnnt1 (A10354, ABclonal), Acta2 (A7248, ABclonal), Myl4 (A13249, ABclonal),
Techniques: Expressing, Recombinant, Plasmid Preparation, Luciferase, RNA Sequencing Assay, Sequencing, Software
Journal: iScience
Article Title: Postnatal expression of cell cycle promoter Fam64a causes heart dysfunction by inhibiting cardiomyocyte differentiation through repression of Klf15
doi: 10.1016/j.isci.2022.104337
Figure Lengend Snippet:
Article Snippet: Primary antibodies used were for Klf15 (NBP2-24635, Novus Biologicals, USA), Trim28 (#4124, Cell Signaling Technology, USA), GR (sc-393232, Santa Cruz Biotechnology, USA), Myh7 (A4963, ABclonal, USA),
Techniques: Expressing, Recombinant, Plasmid Preparation, Luciferase, RNA Sequencing Assay, Sequencing, Software
Journal: International Journal of Molecular Sciences
Article Title: Uncovering the Novel Role of NR1D1 in Regulating BNIP3-Mediated Mitophagy in Ulcerative Colitis
doi: 10.3390/ijms241814222
Figure Lengend Snippet: SR9009 activation of NR1D1 mitigates TNFα-induced cellular pathologies. ( A , B ) Immunoblotting along with semi-quantitative densitometric evaluation for assessing the protein expression of NLRP3 and cleaved caspase-3. ( C ) Representative confocal images illustrating MMP changes, assessed via the JC-1 aggregate:monomer ratio, demonstrate resilience to TNFα-induced MMP loss upon SR9009 treatment, scale bar = 10 μm. ( D , E ) Flow cytometric quantification of ROS via DCFH-DA in CCD841 CoN cells, either siCon- or siNR1D1-pre-treated and TNFα-stimulated, shows ROS attenuation upon SR9009 treatment. ( F ) Apoptosis in CCD841 CoN cells, assessed by flow cytometry following siCon or siNR1D1 and TNFα treatment, is mitigated by SR9009 intervention. Data are presented as means ± standard deviations ( n = 3–6). * p < 0.05, as determined by Student’s t -test.
Article Snippet: Antibodies, reagents, and plasmids: for immunoblotting, antibodies against NR1D1 [#13418S], BMAL1 [#14020S], CLOCK [#5157S], cleaved caspase-3 [#9664S], and GAPDH [#5174S] (Cell Signaling Technology; Danvers, MA, USA); CRY1 [#ab171860],
Techniques: Activation Assay, Western Blot, Expressing, Flow Cytometry
Journal: International Journal of Molecular Sciences
Article Title: Uncovering the Novel Role of NR1D1 in Regulating BNIP3-Mediated Mitophagy in Ulcerative Colitis
doi: 10.3390/ijms241814222
Figure Lengend Snippet: NR1D1, BNIP3, and mitophagy interplay in jet lag and colitis. Jet lag and colitis are hypothesized to cause a decrease in NR1D1 expression in IECs, leading to a concomitant reduction in BNIP3 expression and subsequent impairment of mitophagy. This series of events results in an upregulation of NLRP3 and cleaved caspase-3 expression, driving mitochondrial dysfunction as characterized by a decrease in MMP and an increase in ROS levels. Collectively, these changes promote cellular inflammation and apoptosis, illustrating the complex interplay between circadian disruption, gene expression, and cellular responses in the pathogenesis of jet lag and colitis.
Article Snippet: Antibodies, reagents, and plasmids: for immunoblotting, antibodies against NR1D1 [#13418S], BMAL1 [#14020S], CLOCK [#5157S], cleaved caspase-3 [#9664S], and GAPDH [#5174S] (Cell Signaling Technology; Danvers, MA, USA); CRY1 [#ab171860],
Techniques: Expressing, Disruption