Mitochondrial Membrane Potential Apoptosis Kit, with Mitotracker™ Red & Annexin V Alexa Fluor™ 488, for flow cytometry - Citations

Mitochondrial Membrane Potential Apoptosis Kit, with Mitotracker™ Red & Annexin V Alexa Fluor™ 488, for flow cytometry - Citations

View additional product information for Mitochondrial Membrane Potential Apoptosis Kit, with Mitotracker™ Red & Annexin V Alexa Fluor™ 488, for flow cytometry - Citations (V35116)

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Citations & References
Abstract
Galectin 1 modulates plasma cell homeostasis and regulates the humoral immune response.
AuthorsAnginot A, Espeli M, Chasson L, Mancini SJ, Schiff C,
JournalJ Immunol
PubMed ID23616571
'Galectin-1 (GAL1) is an S-type lectin with multiple functions, including the control of B cell homeostasis. GAL1 expression was reported to be under the control of the plasma cell master regulator BLIMP-1. GAL1 was detected at the protein level in LPS-stimulated B cells and was shown to promote Ig secretion ... More
FGF23 activates injury-primed renal fibroblasts via FGFR4-dependent signalling and enhancement of TGF-ß autoinduction.
AuthorsSmith ER, Holt SG, Hewitson TD
JournalInt J Biochem Cell Biol
PubMed ID28919046
Bone-derived fibroblast growth factor 23 (FGF23) is an important endocrine regulator of mineral homeostasis with effects transduced by cognate FGF receptor (FGFR)1-a-Klotho complexes. Circulating FGF23 levels rise precipitously in patients with kidney disease and portend worse renal and cardiovascular outcomes. De novo expression of FGF23 has been found in the ... More
High Tidal Volume Induces Mitochondria Damage and Releases Mitochondrial DNA to Aggravate the Ventilator-Induced Lung Injury.
AuthorsLin JY, Jing R, Lin F, Ge WY, Dai HJ, Pan L
JournalFront Immunol
PubMed ID30018615
This study aimed to determine whether high tidal volume (HTV) induce mitochondria damage and mitophagy, contributing to the release of mitochondrial DNA (mtDNA). Another aim of the present study was to investigate the role and mechanism of mtDNA in ventilator-induced lung injury (VILI) in rats. ... More
Adaptive phenotypic modulations lead to therapy resistance in chronic myeloid leukemia cells.
AuthorsBaykal-Köse S, Acikgoz E, Yavuz AS, Gönül Geyik Ö, Ates H, Sezerman OU, Özsan GH, Yüce Z
JournalPLoS One
PubMed ID32106243
Tyrosine kinase inhibitor (TKI) resistance is a major problem in chronic myeloid leukemia (CML). We generated a TKI-resistant K562 sub-population, K562-IR, under selective imatinib-mesylate pressure. K562-IR cells are CD34-/CD38-, BCR-Abl-independent, proliferate slowly, highly adherent and form intact tumor spheroids. Loss of CD45 and other hematopoietic markers reveal these cells have ... More