Results 61 to 70 of about 2,802,889 (271)

A simple protocol for the subcellular fractionation of skeletal muscle cells and tissue

open access: yesBMC Research Notes, 2012
Background We describe a method for subcellular fractionation of mouse skeletal muscle, myoblast and myotubes to obtain relatively pure fractions of nuclear, cytosolic and mitochondrial compartments.
Dimauro Ivan   +3 more
doaj   +1 more source

Sensitive detection of fluorescence in western blotting by merging images. [PDF]

open access: yesPLoS ONE, 2018
The western blotting technique is widely used to analyze protein expression levels and protein molecular weight. The chemiluminescence method is mainly used for detection due to its high sensitivity and ease of manipulation, but it is unsuitable for ...
Yukari Kondo   +8 more
doaj   +1 more source

The role of miR‐335‐5p in the redifferentiation of BRAF p.V600E thyroid cancers

open access: yesMolecular Oncology, EarlyView.
The BRAF p.V600E mutation promotes thyroid cancer dedifferentiation and radioiodine resistance. Using a network approach, we identified miR‐335‐5p as a key regulator of BRAF‐mutated thyroid tumors. Restoring miR‐335‐5p increased thyroid‐specific gene expression and iodine uptake in cells and organoids.
Valeria Pecce   +11 more
wiley   +1 more source

IMPDH inhibition enhances cytarabine efficacy in SAMHD1‐expressing leukaemia cells via guanine nucleotide depletion

open access: yesMolecular Oncology, EarlyView.
Cytarabine is a key therapy for acute myeloid leukaemia (AML), but its efficacy is limited by the dNTPase SAMHD1, which hydrolyses its active metabolite. Screening nucleotide biosynthesis inhibitors revealed that IMPDH inhibitors selectively sensitise SAMHD1‐proficient AML cells to cytarabine.
Miriam Yagüe‐Capilla   +9 more
wiley   +1 more source

KDM7A and KDM1A inhibition suppresses tumour promoting pathways in prostate cancer

open access: yesMolecular Oncology, EarlyView.
Treatment resistance is a major challenge for patients with advanced prostate cancer. This study examined an alternative approach to target the major prostate cancer‐promoting pathway by targeting epigenetic factors, whose levels are higher in tumours.
Jennie N Jeyapalan   +16 more
wiley   +1 more source

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

open access: yesMolecular Oncology, EarlyView.
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis   +3 more
wiley   +1 more source

Western String Chamber Orchestra, April 6, 1992

open access: yes, 2016
Recorded during a live performance at Dalton Center Recital Hall, Western Michigan University, Kalamazoo, Michigan, April 6, 1992, 8:00 p.m., the 487th concert of the School of Music’s 1991-1992 season.Western String Chamber Orchestra, Bruce Uchimura ...
Western String Chamber Orchestra
core   +2 more sources

Western String Chamber Orchestra, April 9, 1997

open access: yes, 2016
Recorded during a live performance at Dalton Center Recital Hall, Western Michigan University, Kalamazoo, Michigan, April 9, 1997, 8:00 p.m., the 502nd concert of the School of Music's 1996-1997 season.Western String Chamber Orchestra, Bruce J. Uchimura,
Western String Chamber Orchestra
core   +2 more sources

USP29‐regulated noncanonical stabilization of the hypoxia‐inducible factor‐α in aggressive prostate cancer

open access: yesMolecular Oncology, EarlyView.
We identify USP29 as the only DUB mirroring CA9 expression, a marker of hypoxia and HIF pathway activation associated with PCA aggressiveness. USP29 stabilizes HIF‐1α and HIF‐2α via a noncanonical mechanism that is independent of PHD/pVHL activity yet relies on proteasomal regulation, establishing USP29 as a previously unrecognized regulator of hypoxic
Amelie S Schober   +16 more
wiley   +1 more source

Finding novel vulnerabilities of hypomorphic BRCA1 alleles

open access: yesMolecular Oncology, EarlyView.
Synthetic lethality screens performed to identify novel vulnerabilities often model complete gene loss, thereby overlooking patient‐derived hypomorphic mutations. In this study, we have performed genome‐wide CRISPR screens on BRCA1 hypomorphic mutations, showing BRCA1I26A behaves like wild‐type, while BRCA1R1699Q mimics deficiency. Furthermore, we have
Anne Schreuder   +10 more
wiley   +1 more source

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