Interaction of multiple nuclear proteins with the promoter region of the mouse 68‐kDa neurofilament gene

Abstract

Four brain-specific, DNase I hypersensitive sites (HSS) have been mapped to the 5' flanking region of the mouse 68-kDa neurofilament gene. These sites are contained within a 1.7-kb sequence that confers neuronal specificity of expression of this gene in transgenic mice. To identify DNA sequences that might be involved in gene regulation, the HSS situated near the promoter region has been analyzed by gel mobility shift assays and DNase I footprinting to investigate protein binding sequences. Of particular interest are two footprints localized to a 9-nucleotide sequence that flanks both the light and medium neurofilament gene in mouse and to a sequence that demonstrates partial homology to several promoter regions, including element-1, a motif required for neuron specificity in Drosophila. A prominent footprint was also detected at a sequence that contains a near-perfect palindrome centered at a PstI restriction site.

FLIPL Protects Neurons against In Vivo Ischemia and In Vitro Glucose Deprivation-Induced Cell Death

“…Mice deficient in TNFRI (TNFRI KO) have been described previously (Rothe et al, 1993) and were backcrossed for 12 generations into the C57BL/6 background. For the generation of TgNFL-FLIP L mice, the cDNA encoding for murine FLIP L was cloned downstream of a 1.7 kb 5Ј flanking sequence of the murine neurofilament gene (NFL) that confers neuron-specific expression of heterologous genes (Ivanov and Brown, 1992). Enhanced green fluorescent protein (eGFP) fused to the internal ribosome entry site (IRES) (Clontech, Basingstoke, UK) was cloned downstream of FLIP L to provide an independent protein marker and facilitate screening of the transgenic founders and progeny.…”

Transgenic mouse models of multiple sclerosis

“…Furthermore, the presence of myelin degradation products within phagocytic cells was indicative of an active process. Both studies provide evidence of the detrimental impact of IFN-c on the integrity of the CNS underlining the potential impact of this cytokine in CNS inflammatory a Glial fibrillary acidic protein (GFAP) promotor [265,266] b Neurofilament-light (NF-L) promotor [267,268] c Promoter/distal enhancer of MBP [269] d Proximal promoter/enhancer of MBP [270] e Glial fibrillary acidic protein (GFAP) promotor [271] f Rat neurospecific enolase (NSE) promoter g Glial progenitors (GP) h Oligodendrocytes (ODC) diseases. This is unlikely due to a direct impact of IFN-c on oligodendrocytes as IFN-c is not directly cytotoxic for cultured oligodendrocytes [190].…”

Intermediate filaments: regulation of gene expression and assembly

“…Recently the 1.7-kb mouse NF-L 5'-upstream region has been investigated for the presence of hypersensitive regions (Ivanov and Brown 1992). Nuclear extracts prepared from brain and liver nuclei have been used for the mapping of hypersensitive regions.…”