Results 61 to 70 of about 30,395 (278)

Large-scale population study of human cell lines indicates that dosage compensation is virtually complete. [PDF]

open access: yesPLoS Genetics, 2008
X chromosome inactivation in female mammals results in dosage compensation of X-linked gene products between the sexes. In humans there is evidence that a substantial proportion of genes escape from silencing.
Colette M Johnston   +5 more
doaj   +1 more source

BMT4me En Español: Multisite Feasibility and Usability Testing of a Spanish‐Language mHealth Adherence Support App for Spanish‐Speaking Caregivers of Children After Hematopoietic Stem Cell Transplantation and Cancer Treatment

open access: yesPediatric Blood &Cancer, EarlyView.
ABSTRACT Background Medication nonadherence during the first 100 days after pediatric hematopoietic stem cell transplantation (HSCT) and during oncology treatment increases risk for complications. BMT4me is a caregiver‐facing mobile health (mHealth) application providing medication reminders, symptom tracking, and note‐taking features to support ...
Micah A. Skeens   +4 more
wiley   +1 more source

Absence of X-chromosome dosage compensation in the primordial germ cells of Drosophila embryos

open access: yesScientific Reports, 2021
Dosage compensation is a mechanism that equalizes sex chromosome gene expression between the sexes. In Drosophila, individuals with two X chromosomes (XX) become female, whereas males have one X chromosome (XY).
Ryoma Ota   +4 more
doaj   +1 more source

Condensin function in dosage compensation [PDF]

open access: yesEpigenetics, 2009
Dosage compensation is an essential process that equalizes X-linked gene dosage between the sexes. In the worm Caenorhabditis elegans, a complex of proteins called the dosage compensation complex (DCC) binds both X chromosomes in hermaphrodites to downregulate gene expression two-fold and hence to reduce X-linked gene expression levels equal to that in
openaire   +2 more sources

Bridging the Gap in Neuroblastoma Care: Consensus‐Based Statements With Recommendations for Improved Patient and Caregiver Experiences

open access: yesPediatric Blood &Cancer, EarlyView.
ABSTRACT Neuroblastoma's complex, heterogeneous biology poses significant diagnostic and therapeutic challenges, often requiring caregivers to absorb complex information and participate in time‐sensitive decisions. However, caregivers often feel unprepared to evaluate options.
Vickie Buenger   +8 more
wiley   +1 more source

A sequence motif enriched in regions bound by the Drosophila dosage compensation complex

open access: yesBMC Genomics, 2010
Background In Drosophila melanogaster, dosage compensation is mediated by the action of the dosage compensation complex (DCC). How the DCC recognizes the fly X chromosome is still poorly understood.
Aldecoa Rodrigo   +3 more
doaj   +1 more source

An epithelial GPR35 isoform supports tumor‐associated transcriptional and metabolic phenotypes

open access: yesFEBS Letters, EarlyView.
GPR35 generates two functionally distinct isoforms with previously unresolved roles. GPR35‐short mediates immune‐cell chemotaxis, while GPR35‐long is enriched in colorectal cancer epithelium, where it supports increased metabolism, proliferation, and tumor‐associated transcriptional programs.
Jørgen D. Rønneberg   +14 more
wiley   +1 more source

Regional differences in dosage compensation on the chicken Z chromosome [PDF]

open access: yes, 2007
BackgroundMost Z chromosome genes in birds are expressed at a higher level in ZZ males than in ZW females, and thus are relatively ineffectively dosage compensated. Some Z genes are compensated, however, by an unknown mechanism.
Esther Melamed   +3 more
core   +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

Dosage compensation can buffer copy-number variation in wild yeast

open access: yeseLife, 2015
Aneuploidy is linked to myriad diseases but also facilitates organismal evolution. It remains unclear how cells overcome the deleterious effects of aneuploidy until new phenotypes evolve. Although laboratory strains are extremely sensitive to aneuploidy,
James Hose   +5 more
doaj   +1 more source

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