Results 91 to 100 of about 332,161 (328)
From Linear Genes to Epigenetic Inheritance of Three-dimensional Epigenomes [PDF]
, 2011 Fifty years ago Jacob and Monod reported their findings on the regulation of gene activity. Working on lambda bacteriophage lysogeny and the regulation of the production of an enzyme that cleaves lactose, they observed that its production was induced by ...
Cavalli, Giacomo
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Molecular Oncology, EarlyView.Combining PTEN protein assessment and transcriptomic profiling of prostate tumors, we uncovered a network enriched in senescence and extracellular matrix (ECM) programs associated with PTEN loss and conserved in a mouse model. We show that PTEN‐deficient cells trigger paracrine remodeling of the surrounding stroma and this information could help ...
Ivana Rondon‐Lorefice +16 more
wiley +1 more source
Partial dosage compensation in Strepsiptera, a sister group of beetles. [PDF]
, 2015 Sex chromosomes have evolved independently in many different taxa, and so have mechanisms to compensate for expression differences on sex chromosomes in males and females. Different clades have evolved vastly different ways to achieve dosage compensation,
Bachtrog, Doris, Mahajan, Shivani
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Molecular Oncology, EarlyView.We show that the majority of the 18 analyzed recurrent cancer‐associated ERBB4 mutations are transforming. The most potent mutations are activating, co‐operate with other ERBB receptors, and are sensitive to pan‐ERBB inhibitors. Activating ERBB4 mutations also promote therapy resistance in EGFR‐mutant lung cancer.
Veera K. Ojala +15 more
wiley +1 more source
Peroxidasin enables melanoma immune escape by inhibiting natural killer cell cytotoxicity
Molecular Oncology, EarlyView.Peroxidasin (PXDN) is secreted by melanoma cells and binds the NK cell receptor NKG2D, thereby suppressing NK cell activation and cytotoxicity. PXDN depletion restores NKG2D signaling and enables effective NK cell–mediated melanoma killing. These findings identify PXDN as a previously unrecognized immune evasion factor and a potential target to improve
Hsu‐Min Sung +17 more
wiley +1 more source
BMC GenomicsBackground X-chromosome inactivation (XCI) is an epigenetic process that occurs during early development in mammalian females by randomly silencing one of two copies of the X chromosome in each cell.
Numrah Fadra +11 more
doaj +1 more source
Epigenetics & Chromatin, 2008 Background X chromosome inactivation is the mechanism used in mammals to achieve dosage compensation of X-linked genes in XX females relative to XY males. Chromosome silencing is triggered in cis by expression of the non-coding RNA Xist. As such, correct
Nesterova Tatyana B +10 more
doaj +1 more source
ProtocadherinX/Y, a Candidate Gene-Pair for Schizophrenia and Schizoaffective Disorder: A DHPLC Investigation of Gonomic Sequence [PDF]
, 2004 Protocadherin X and Protocadherin Y (PCDHX and PCDHY) are cell-surface adhesion molecules expressed predominantly in the brain. The PCDHX/Y gene-pair was generated by an X-Y translocation approximately 3 million years ago (MYA) that gave rise to the Homo
Crow, Prof TJ +4 more
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Redox regulation meets metabolism: targeting PRDX2 to prevent hepatocellular carcinoma
Molecular Oncology, EarlyView.PRDX2 acts as a central redox hub linking metabolic dysfunction‐associated steatohepatitis (MASH) to hepatocellular carcinoma (HCC). In normal hepatocytes, PRDX2 maintains redox balance and metabolic homeostasis under oxidative stress. In contrast, during malignant transformation, PRDX2 promotes oncogenic signaling, stemness, and tumor initiation ...
Naroa Goikoetxea‐Usandizaga +2 more
wiley +1 more source
Clonal Composition of Human Adrenocortical Neoplasms [PDF]
, 1994 The mechanisms of tumorigenesis of adrenocortical neoplasms are still not understood. Tumor formation may be the result of spontaneous transformation of adrenocortical cells by somatic mutations.
Abdelhamid, S. +7 more
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