This SuperSeries is composed of the SubSeries listed below.
Metabolic pathway profiling of mitochondrial respiratory chain mutants in C. elegans.
No sample metadata fields
View SamplesUtilizing C. elegans as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of hypomorhpic C. elegans mutants in nuclear-encoded subunits of respiratory chain complexes I, II and III.
Metabolic pathway profiling of mitochondrial respiratory chain mutants in C. elegans.
No sample metadata fields
View SamplesUtilizing C. elegans as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of hypomorphic C. ele
Metabolic pathway profiling of mitochondrial respiratory chain mutants in C. elegans.
No sample metadata fields
View SamplesUtilizing M. musculus as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of liver-conditional knockout mice for Pdss2 compared with loxP controls.
Primary coenzyme Q deficiency in Pdss2 mutant mice causes isolated renal disease.
No sample metadata fields
View SamplesCD34+ human cord blood-derived cells were subjected to GFP mRNA delivery or mock treatment using Centrifugation enhanced Nanostraw Transfection (CeNT) or conventional electroporation.
Efficient and nontoxic biomolecule delivery to primary human hematopoietic stem cells using nanostraws.
Specimen part, Treatment
View SamplesRNA sequencing of ILC2s sorted from ß2 adrenergic receptor agonist-treated and non-treated mice Overall design: RNAs of ILC2s sorted as KLRG1+CD127+CD90+Lin-CD45+ from ß2 adrenergic receptor agonist-treated and non-treated mice mLNs 4 days post N. brasiliensis infection were analyzed
β<sub>2</sub>-adrenergic receptor-mediated negative regulation of group 2 innate lymphoid cell responses.
Specimen part, Cell line, Treatment, Subject
View SamplesWe provide a map of human ILC heterogeneity across multiple anatomical sites. Tissue-specific distinctions are particularly apparent for ILC1 populations, whose distribution was markedly altered in obesity or aging. Furthermore, the degree of ILC1 population hetero- geneity differed substantially in lymphoid versus mucosal sites. Together, these analyses comprise a comprehensive characterization of the spatial and temporal dynamics regulating the anatomical distri- bution, subset heterogeneity, and functional poten- tial of ILCs in non-diseased human tissues. Overall design: We present a quantitative analysis of ILC distribution and heterogeneity in lymphoid, mucosal, and metabolic tissues obtained from a diverse cohort of 44 previously non-diseased organ donors over a wide range of ages and body mass indexes (BMIs).
Spatial and Temporal Mapping of Human Innate Lymphoid Cells Reveals Elements of Tissue Specificity.
Specimen part, Subject
View SamplesThe liver stage of the etiological agent of malaria, Plasmodium, is obligatory for successful infection of its various mammalian hosts. Differentiation of the rod-shaped sporozoites of Plasmodium into spherical exoerythrocytic forms (EEFs) via bulbous expansion is essential for parasite development in the liver. However, little is known about the host factors regulating the morphological transformation of Plasmodium sporozoites in this organ. Here, we show that sporozoite differentiation into EEFs in the liver involves protein kinase C?-mediated NF-?B activation, which robustly induces the expression of C-X-C chemokine receptor type 4 (CXCR4) in hepatocytes and subsequently elevates intracellular Ca2+ levels, thereby triggering sporozoite transformation into EEFs. Blocking CXCR4 expression by genetic or pharmacological intervention profoundly inhibited the liver stage development of the P. berghei rodent malaria parasite and the human P. falciparum parasite also. Collectively, our experiments show that CXCR4 is a key host factor for Plasmodium development in the liver, and CXCR4 warrants further investigation for malaria prophylaxis. Overall design: To explore the molecular mechanisms by which the HGF/MET/PKC?/NF-?B pathway regulates P. berghei sporozoite development in hepatocytes, we compared the gene expression patterns in wild-type and PKC?-KO Huh7 cells treated or not treated with HGF. We also analyzed the gene expression profiles in wild type and PKC?-KO Huh7 cells uninfected or infected with P. berghei sporozoites.
CXCR4 regulates <i>Plasmodium</i> development in mouse and human hepatocytes.
Specimen part, Subject
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