publication_authors:Kawakami H Results

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Microarray (447)

Platform

Affymetrix Human Gene 1.1 ST Array (hugene11st) (285)

Affymetrix Mouse Genome 430 2.0 Array (mouse4302) (162)

Includes Publication

GSE8555

Genome-wide analysis of Phgdh inactivation in murine embryonic head

Mus musculus
4 Downloadable Samples

Description

D-3-Phosphoglycerate dehydrogenase (Phgdh; EC 1.1.1.95) is a necessary enzyme for de novo L-serine biosynthesis via the phosphorylated pathway. We demonstrated previously that Phgdh is expressed exclusively by neuroepithelium and radial glia in developing mouse brain and later mainly by astrocytes. Mutations in the human PHGDH gene cause serine deficiency disorders (SDD) associated with severe neurological symptoms such as congenital microcephaly, psychomotor retardation, and intractable seizures. We recently demonstrated that genetically engineered mice, in which the gene for Phgdh has been disrupted, have significantly decreased levels of serine and glycine, and exhibit malformation of brain such as microcephaly. The Phgdh null (KO) embryos exhibit lethal phenotype after gestational day 14, indicating that the phosphorylated pathway is essential for embryogenesis, especially for brain development. It is worth noting that the Phgdh knockout (KO) embryos primarily displayed microcephaly, which is the most conspicuous phenotype of patients with SDD. Thus, Phgdh KO mice are a useful animal model for studying the effect of diminished L-serine levels on development of the central nervous system and other organs. To better understand the mechanism underlying the molecular pathogenesis of SDD, we sought to examine whether gene expression is altered in the Phgdh KO mouse model. We identify genes that have altered expression in the head of the Phgdh KO embryos using the GeneChip array. Some of the genes identified by this method belong in functional categories that are relevant to the biochemical and morphological aberrations of the Phgdh deletion.

Publication Title

Inactivation of the 3-phosphoglycerate dehydrogenase gene in mice: changes in gene expression and associated regulatory networks resulting from serine deficiency.

Sample Metadata Fields

Specimen part

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GSE25029

Ionizing radiation in GI tract of Tweak KO mice

Mus musculus
54 Downloadable Samples

Description

TWEAK/Fn14 signaling may regulate the expression of genes involved in epithelial repair and mucosal inflammation. Comparing the gene signatures in WT and TWEAK KO mice will inform the biology of TWEAK/Fn14 pathway in the GI tract.

Publication Title

Interleukin-13 damages intestinal mucosa via TWEAK and Fn14 in mice-a pathway associated with ulcerative colitis.

Sample Metadata Fields

Specimen part, Treatment

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GSE33106

Expression data from livers in wildtype and Sox17+/-mice at 17dpc

Mus musculus
4 Downloadable Samples

Description

The onset of the liver inflamentation in the Sox17+/- embryos.

Publication Title

Sox17 haploinsufficiency results in perinatal biliary atresia and hepatitis in C57BL/6 background mice.

Sample Metadata Fields

Specimen part

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GSE10765

Expression data from MALP-2-stimulated macrophages from wild-type, IRAK-2-/- and IRAK-1-/IRAK-2-/- mice

Mus musculus
12 Downloadable Samples

Description

IL-1R-associated kinases (IRAKs) participate in Toll-like receptor (TLR) signal transduction. MALP-2 is a TLR2 ligand, and stimulation of macrophages with MALP-2 activates expression of various genes including proinflammatory cytokines.

Publication Title

Sequential control of Toll-like receptor-dependent responses by IRAK1 and IRAK2.

Sample Metadata Fields

No sample metadata fields

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GSE95278

Skin inflammation exacerbates food allergy symptoms in epicutaneously sensitized mice

Mus musculus
4 Downloadable Samples

Description

Cutaneous exposure to food antigen through impaired skin barrier has been shown to induce epicutaneous sensitization, and thereby cause IgE-mediated food allergy.

Publication Title

Skin inflammation exacerbates food allergy symptoms in epicutaneously sensitized mice.

Sample Metadata Fields

Sex, Specimen part

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GSE22448

Gene expression data from wild-type and Nlrc5 knockout GM-CSF induced bone marrow dendritic cells infected with Newcastle Disease virus.

Mus musculus
6 Downloadable Samples

Description

Nlrc5 is encoding a Nod-like receptor protein NLRC5/NOD27. To check the involvement of Nlrc5 in antiviral response, we examined gene expression profile in wild-type and Nlrc5 knockout GM-CSF bone marrow macrophage with using microarrays.

Publication Title

NLRC5 deficiency does not influence cytokine induction by virus and bacteria infections.

Sample Metadata Fields

Specimen part, Time

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GSE62648

Gene expression profiles in dorsal skin of hairless mice orally administrated collagen hydrolysate for 1 week

Mus musculus
8 Downloadable Samples

Description

Dietary collagen hydrolysate has been conjectured to improve skin barrier function. To investigate the effect of long-term collagen hydrolysate administration on the skin, we evaluated stratum corneum water content and skin elasticity in intrinsic aged mice. Female 9-week-old hairless mice were fed a control diet, or a collagen hydrolysate-containing diet, for 12 weeks. The stratum corneum water content and skin elasticity were sequentially decreased by chronological aging in control mice. Intake of collagen hydrolysate significantly suppressed such changes. Moreover, we comprehensively analyzed gene expression in the skin of mouse, which had been administered collagen hydrolysate, using DNA microarray. Twelve weeks after start of collagen intake, no significant differences appeared in gene expression profile compared to that of control group. However, 1 week after administration, 135 genes were up-regulated and 448 genes were down-regulated in collagen group compared to control group. It is indicate that gene changes preceded changes of barrier function and elasticity. We focused on several genes correlated with functional changes in the skin. Gene Ontology terms, especially related to epidermal cell development, were signicantly enriched in up-regulated genes. These skin function-related genes had properties that facilitate epidermal production and differentiation and suppress dermal degradation. Thus, dietary collagen hydrolysate induced positive gene changes. In conclusion, our results suggest that alteration of gene expression at early stages after collagen administration affect skin barrier function and mechanical properties. Long-term oral intake of collagen hydrolysate improves skin dysfunction by regulating genes related to production and maintenance of the skin tissue.