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Transcription profiling of mouse livers from growth hormone receptor (GHR) deficient mice and mice expressing different forms of truncated GHR to study the GHR signaling domains and their associated transcripts.

ABSTRACT: Total RNA was extracted from mouse liver samples using an Ambion RNaqueous RNA extraction kit. Targets were produced using modified Affymetrix procedure from 5ug of total RNA. 3 biological replicates were analysed per each group of animals.

ORGANISM(S): Mus musculus

SUBMITTER: Agnieszka Maria Lichanska

PROVIDER: E-GEOD-988 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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In vivo analysis of growth hormone receptor signaling domains and their associated transcripts.

Rowland Jennifer E JE Lichanska Agnieszka M AM Kerr Linda M LM White Mary M d'Aniello Elisabetta M EM Maher Sheryl L SL Brown Richard R Teasdale Rohan D RD Noakes Peter G PG Waters Michael J MJ

Molecular and cellular biology 20050101 1

The growth hormone receptor (GHR) is a critical regulator of postnatal growth and metabolism. However, the GHR signaling domains and pathways that regulate these processes in vivo are not defined. We report the first knock-in mouse models with deletions of specific domains of the receptor that are required for its in vivo actions. Mice expressing truncations at residue m569 (plus Y539/545-F) and at residue m391 displayed a progressive impairment of postnatal growth with receptor truncation. More ...[more]

PMID: 15601831

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mouse liver samples

Project description:Total RNA was extracted from mouse liver samples using an Ambion RNaqueous RNA extraction kit. Targets were produced using modified Affymetrix procedure from 5ug of total RNA. 3 biological replicates were analysed per each group of animals. Keywords = growth hormone Keywords = signaling Keywords = gene expression Keywords: other

2005-01-01 | GSE988 | GEO

Comparison of transcripts from the anterior tibialis, gastrocnemius, and liver of glycogen synthase WT, GSL30 or KO mice

Project description:Anterior tibialis removed from 3-month old muscle glycogen synthase WT or knockout mouse. RNA was extracted using GibcoBRL TRIzol Reagent and a Quiagen RNeasy kit. Targets were produced using standard Affymetrix procedures from about 5ug of total RNA. GSM40057-GSM40063 AND GSM40956. Liver removed from 3-month old muscle glycogen synthase WT or knockout mouse. RNA was extracted using GibcoBRL TRIzol Reagent and a Quiagen RNeasy kit. Targets were produced using standard Affymetrix procedures from about 10ug of total RNA. GSM40064-GSM40071. Medial gastrocnemius removed from 3-month old muscle glycogen synthase WT or knockout mouse. RNA was extracted using GibcoBRL TRIzol Reagent and a Quiagen RNeasy kit. Targets were produced using standard Affymetrix procedures from about 5ug of total RNA. GSM40072-GSM40079. Medial gastrocnemius removed from 8-month old muscle glycogen synthase WT or overexpressing mouse. RNA was extracted using GibcoBRL TRIzol Reagent and a Quiagen RNeasy kit. Targets were produced using standard Affymetrix procedures from about 5ug of total RNA. GSM40080-GSM40089 Keywords: other

2006-01-27 | GSE2198 | GEO

RNA-sequencing of Control and Bisphenol A (BPA) exposed mice livers.

Project description:To elucidate the molecular perturbations underlying the connection of low-dose prenatal BPA exposure to cardiometabolic diseases, we assessed the liver transcriptome in both male and female mouse offspring exposed to 5ug/kg/day BPA and corn oil (control) during gestation.

2020-12-01 | GSE155845 | GEO

In vivo analysis of growth hormone receptor signaling domains and their associated transcripts.

Project description:The growth hormone receptor (GHR) is a critical regulator of postnatal growth and metabolism. However, the GHR signaling domains and pathways that regulate these processes in vivo are not defined. We report the first knock-in mouse models with deletions of specific domains of the receptor that are required for its in vivo actions. Mice expressing truncations at residue m569 (plus Y539/545-F) and at residue m391 displayed a progressive impairment of postnatal growth with receptor truncation. Moreover, after 4 months of age, marked male obesity was observed in both mutant 569 and mutant 391 and was associated with hyperglycemia. Both mutants activated hepatic JAK2 and ERK2, whereas STAT5 phosphorylation was substantially decreased for mutant 569 and absent from mutant 391, correlating with loss of IGF-1 expression and reduction in growth. Microarray analysis of these and GHR(-/-) mice demonstrated that particular signaling domains are responsible for the regulation of different target genes and revealed novel actions of growth hormone. These mice represent the first step in delineating the domains of the GHR regulating body growth and composition and the transcripts associated with these domains.

| S-EPMC538772 | biostudies-literature

Cancer cells express aberrant DNMT3B transcripts encoding truncated proteins.

Project description:Cancer cells display an altered distribution of DNA methylation relative to normal cells. Certain tumor suppressor gene promoters are hypermethylated and transcriptionally inactivated, whereas repetitive DNA is hypomethylated and transcriptionally active. Little is understood about how the abnormal DNA methylation patterns of cancer cells are established and maintained. Here, we identify over 20 DNMT3B transcripts from many cancer cell lines and primary acute leukemia cells that contain aberrant splicing at the 5' end of the gene, encoding truncated proteins lacking the C-terminal catalytic domain. Many of these aberrant transcripts retain intron sequences. Although the aberrant transcripts represent a minority of the DNMT3B transcripts present, Western blot analysis demonstrates truncated DNMT3B isoforms in the nuclear protein extracts of cancer cells. To test if expression of a truncated DNMT3B protein could alter the DNA methylation patterns within cells, we expressed DNMT3B7, the most frequently expressed aberrant transcript, in 293 cells. DNMT3B7-expressing 293 cells have altered gene expression as identified by microarray analysis. Some of these changes in gene expression correlate with altered DNA methylation of corresponding CpG islands. These results suggest that truncated DNMT3B proteins could play a role in the abnormal distribution of DNA methylation found in cancer cells.

| S-EPMC2435620 | biostudies-literature

H3K27ac and H3K4me3 ChIP-Seq of livers from male mice fed a control or high-fat diet and treated with estrogen receptor agonists

Project description:Metabolic dysfunction-associated steatotic liver disease is the most prevalent liver disease and affects a quarter of the global population. Estrogens are associated to safeguard the liver from metabolic diseases. We fed male mice a control or high-fat diet for 13 weeks which induced fatty liver. We injected a subset of male mice fed a high-fat diet with four different estrogen receptor (ER) agonists for the last three weeks of the high-fat diet, activating ERalpha or ERbeta. Livers were collected and crosslinked using formaldehyde. ChIP-seq against H3K27ac (Abcam #4729, 5ug per IP) or H3K4me3 (Merck 05-1339, 5ug per IP) was performed, followed by library preparation and sequencing on an Illumina NextSeq 500 instrument. RNA-seq of the same individual mice was performed and is accessible under E-MTAB-11833. The mouse identification column ('Sample' followed by number) can be used to match the individual mice between the experiments.

2024-02-22 | E-MTAB-11929 | biostudies-arrayexpress

Expression data from developing mouse livers

Project description:Roles of mesothelial cells (MCs) are poorly understood during liver development and injury. We identified podoplanin (Pdpn) as a cell surface markers for mesothelial cells in E12.5 mouse developing liver. To identify genes uniquely expressed in MCs, we isolated MCs from E12.5 mouse livers by FACS using anti-Pdpn antibodies and performed microarray analysis. The E12.5 liver was digested with trypsin-EDTA and incubated with antibodies against Pdpn. MCs were isolated as Pdpn+ population by FACS. Total RNA was extracted with RNAqueous Micro (Ambion) and the probes for the microarray were synthesized using the Ovation RNA amplification system V2 and FL-Ovation cDNA Biotin module V2 (Nugen). The labeled probes were hybridized with GeneChip Mouse Genome 430 2.0 arrays (Affymetrix) and signals were analyzed with Genomic Suite software (Partek).

2013-02-04 | E-GEOD-39064 | biostudies-arrayexpress

Truncated forms of human complement factor H.

Project description:By the use of Western-blot analyses with polyclonal anti-(Factor H) antibodies, two low-Mr protein species of Mr 41,000 and 37,000 under non-reducing conditions and 43,000 and 40,000 under reducing conditions are consistently detected together with the well-known 155,000-Mr Factor H in human plasma and serum. These two additional species are also found in plasma, urine and synovial fluids. The 41,000-Mr species but not the 37,00-Mr species is detected by a monoclonal anti-(Factor H) antibody directed at the N-terminal part of Factor H. The 37,000-Mr species but not the 41,000-Mr species is detected by a monoclonal anti-(Factor H) antibody directed at the C-terminal part of Factor H. The 41,000-Mr and 37,000-Mr species are different from the well-characterized 36,000-Mr N-terminal tryptic fragment of Factor H. They are likely to represent translational products of the short Factor H mRNA species of 1.8 kb and 1.2-1.5 kb occurring in human liver that we have recently described.

| S-EPMC1138455 | biostudies-other

Reduced autophagy in livers of fasted, fat-depleted, ghrelin-deficient mice: reversal by growth hormone.

Project description:Plasma growth hormone (GH) and hepatic autophagy each have been reported to protect against hypoglycemia in the fasted state, but previous data have not linked the two. Here we demonstrate a connection using a mouse model of fasting in a fat-depleted state. Mice were subjected to 1 wk of 60% calorie restriction, causing them to lose nearly all body fat. They were then fasted for 23 h. During fasting, WT mice developed massive increases in plasma GH and a concomitant increase in hepatic autophagy, allowing them to maintain viable levels of blood glucose. In contrast, lethal hypoglycemia occurred in mice deficient in the GH secretagogue ghrelin as a result of knockout of the gene encoding ghrelin O-acyltransferase (GOAT), which catalyzes a required acylation of the peptide. Fasting fat-depleted Goat(-/-) mice showed a blunted increase in GH and a marked decrease in hepatic autophagy. Restoration of GH by infusion during the week of calorie restriction maintained autophagy in the Goat(-/-) mice and prevented lethal hypoglycemia. Acute injections of GH after 7 d of calorie restriction also restored hepatic autophagy, but failed to increase blood glucose, perhaps owing to ATP deficiency in the liver. These data indicate that GH stimulation of autophagy is necessary over the long term, but not sufficient over the short term to maintain blood glucose levels in fasted, fat-depleted mice.

| S-EPMC4313810 | biostudies-other

Inhibition of Sodium Ion Channel Function with Truncated Forms of Batrachotoxin.

Project description:A novel family of small molecule inhibitors of voltage-gated sodium channels (NaVs) based on the structure of batrachotoxin (BTX), a well-known channel agonist, is described. Protein mutagenesis and electrophysiology experiments reveal the binding site as the inner pore region of the channel, analogous to BTX, alkaloid toxins, and local anesthetics. Homology modeling of the eukaryotic channel based on recent crystallographic analyses of bacterial NaVs suggests a mechanism of action for ion conduction block.

| S-EPMC5555364 | biostudies-literature

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