Impaired SNF2L Chromatin Remodeling Prolongs Accessibility at Promoters Enriched for Fos/Jun Binding Sites and Delays Granule Neuron Differentiation.

Chromatin remodeling proteins utilize the energy from ATP hydrolysis to mobilize nucleosomes often creating accessibility for transcription factors within gene regulatory elements. Aberrant chromatin remodeling has diverse effects on neuroprogenitor homeostasis altering progenitor competence, proliferation, survival, or cell fate. Previous work has shown that inactivation of the genes, (encoding Snf2h) and (encoding Snf2l) have dramatic effects on brain development.

Characterization of molecular attributes that influence LINE-1 restriction by all seven human APOBEC3 proteins.

LINE-1 (L1) is a non-long terminal repeat (LTR) retrotransposon inserted throughout the human genome. APOBEC3 (A3) proteins are part of a network of host intrinsic defenses capable of restricting retroviruses and the replication of L1 retroelements. These enzymes inactivate retroviruses primarily through deamination of single-stranded viral DNA.

The role of ISWI chromatin remodeling complexes in brain development and neurodevelopmental disorders.

The mammalian ISWI (Imitation Switch) genes SMARCA1 and SMARCA5 encode the ATP-dependent chromatin remodeling proteins SNF2L and SNF2H. The ISWI proteins interact with BAZ (bromodomain adjacent to PHD zinc finger) domain containing proteins to generate eight distinct remodeling complexes. ISWI complex-mediated nucleosome positioning within genes and gene regulatory elements is proving important for the transition from a committed progenitor state to a differentiated cell state.

Stat-6 signaling pathway and not Interleukin-1 mediates multi-walled carbon nanotube-induced lung fibrosis in mice: insights from an adverse outcome pathway framework.

Background: The accumulation of MWCNTs in the lung environment leads to inflammation and the development of disease similar to pulmonary fibrosis in rodents. Adverse Outcome Pathways (AOPs) are a framework for defining and organizing the key events that comprise the biological changes leading to undesirable events. A putative AOP has been developed describing MWCNT-induced pulmonary fibrosis; inflammation and the subsequent healing response induced by inflammatory mechanisms have been implicated in disease progression.