Disease relevance of Cigs1

• Il4 gene accessibility, analyzed by restriction enzyme accessibility (REA) at sites in the promoter, in the second intron (DNase I hypersensitivity sites HSII and HSIII) and in CNS-1 in the two populations was also similar [1].
• We demonstrate that treatment with hsFlt3L leads to inhibition of tumor growth and significantly increased life span of animals implanted with syngeneic CNS-1 glioma cells [2].
• Conservation of CNS1 and exclusion of its role in atopic eczema susceptibility [3].
• These include a CCAAT box at HSS2, a novel brain-specific footprint near an adenovirus promoter element E2aE-C beta and a single liver-specific footprint associated with an POU/octamer binding site at HSS4 [4].

High impact information on Cigs1

• Thus, monoallelism at the Il4 locus is a complex process; expression is linked to opening CNS1 but probability of expression is controlled at other sites [5].
• Here we describe the phenotype of mice in which hypersensitive sites 1 and 2 (HSS1 and 2) of DNaseI hypersensitive Cluster II (CII), which are located upstream of the CD8 alpha gene, were deleted by targeted homologous recombination of the endogenous locus [6].
• Conserved noncoding sequence elements longer than 80 bp with >/=75% nucleotide sequence identity comprise approximately 1% of the genomic sequence in this region [7].
• Cns-1 transcripts are expressed in differentiating cells cultured from the early postnatal cerebellum [8].
• The NMDA-induced increase in Cns-1 mRNA was reduced by pretreatment with calcium chelators EGTA or 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA) tetrakis(acetoxymethyl) [8].

Chemical compound and disease context of Cigs1

• Mimosine-treated neural precursor cells injected into established intracerebral CNS-1 gliomas in nude mice migrated extensively throughout the tumor and into the surrounding parenchyma beyond the tumor over 3 days [9].

Biological context of Cigs1

• However, the replication timing of this locus is consistently early during S phase in both Th1 and Th2 cells under either the wild-type or CNS-1 deletion background [10].
• These studies suggest that specific activation of the NMDA receptor in cultures of differentiating cerebellar cells increases Cns-1 gene expression and that calcium entry through the NMDA channel may be required for this response [8].
• The sequences associated with hypersensitive site 1 (HSS1) represented the principal area of homology within which three conserved subdomains were apparent: area I (-2694 to -2561 base pairs (bp)), area II (-2139 to -1958 bp), and area III (-1879 to -1799 bp) [11].
• The human Iglambda enhancer consists of three separated sequence elements that we identified previously by mapping DNase I-hypersensitive regions (HSS) downstream of the C region of the Iglambda L chain genes (HSS-1, HSS-2, and HSS-3) [12].
• Three DNase I-hypersensitive sites (HSS0, HSS1 and HSS2) have been described upstream of the rabbit WAP gene in the lactating mammary gland and correspond to important regulatory regions [13].

Anatomical context of Cigs1

• Despite the profound effect in T cells, mast cells from CNS-1(-/-) mice maintained their capacity to produce interleukin 4 [14].
• This showed that CNS-1 and CNS-2 have differential transcriptional regulatory activity in epithelial cell lines [15].

Associations of Cigs1 with chemical compounds

• Mimosine-treated neural precursor cells, infected with rRp450 and injected into intracerebral CNS-1 tumors, also migrated within the tumor with the appearance of foci of HSV-thymidine kinase-positive (TK+) cells, presumably including tumor cells, distributed throughout the tumor and in the surrounding parenchyma over a similar period [9].

Other interactions of Cigs1

• Like CD4(-/-) and Itk(-/-) mice, CNS-1(-/-) BALB/c mice were highly resistant to the Th2-inducing protozoan, Leishmania major [16].
• Characterization of a human multilineage-colony-stimulating factor cDNA clone identified by a conserved noncoding sequence in mouse interleukin-3 [17].

Analytical, diagnostic and therapeutic context of Cigs1

• NMDA receptor activation in differentiating cerebellar cell cultures regulates the expression of a new POU gene, Cns-1 [8].
• In addition, by chromatin immunoprecipitation assay, we show that GR is rapidly recruited to endogenous CNS-1 chromatin after GC stimulation [18].
• CpG-ODNs had no effect on a s.c. CNS1 tumor in nude mice, which suggested that CpG-ODN is not directly cytotoxic and that immunostimulation is required for the antitumoral effect [19].
• Gel mobility shift assays revealed a similar but not identical banding pattern with brain and liver nuclear extracts at HSS2, and HSS3, however the banding pattern for HSS4 was predominantly brain-specific [4].

References