ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Publication Date: 2008-08-23
    Description: Brown fat can increase energy expenditure and protect against obesity through a specialized program of uncoupled respiration. Here we show by in vivo fate mapping that brown, but not white, fat cells arise from precursors that express Myf5, a gene previously thought to be expressed only in the myogenic lineage. We also demonstrate that the transcriptional regulator PRDM16 (PRD1-BF1-RIZ1 homologous domain containing 16) controls a bidirectional cell fate switch between skeletal myoblasts and brown fat cells. Loss of PRDM16 from brown fat precursors causes a loss of brown fat characteristics and promotes muscle differentiation. Conversely, ectopic expression of PRDM16 in myoblasts induces their differentiation into brown fat cells. PRDM16 stimulates brown adipogenesis by binding to PPAR-gamma (peroxisome-proliferator-activated receptor-gamma) and activating its transcriptional function. Finally, Prdm16-deficient brown fat displays an abnormal morphology, reduced thermogenic gene expression and elevated expression of muscle-specific genes. Taken together, these data indicate that PRDM16 specifies the brown fat lineage from a progenitor that expresses myoblast markers and is not involved in white adipogenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2583329/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2583329/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seale, Patrick -- Bjork, Bryan -- Yang, Wenli -- Kajimura, Shingo -- Chin, Sherry -- Kuang, Shihuan -- Scime, Anthony -- Devarakonda, Srikripa -- Conroe, Heather M -- Erdjument-Bromage, Hediye -- Tempst, Paul -- Rudnicki, Michael A -- Beier, David R -- Spiegelman, Bruce M -- R01 AR044031/AR/NIAMS NIH HHS/ -- R01 AR044031-11/AR/NIAMS NIH HHS/ -- R37 DK031405/DK/NIDDK NIH HHS/ -- R37 DK031405-27/DK/NIDDK NIH HHS/ -- England -- Nature. 2008 Aug 21;454(7207):961-7. doi: 10.1038/nature07182.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute and the Department of Cell Biology, Harvard Medical School, 1 Jimmy Fund Way, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18719582" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes, Brown/cytology/*metabolism ; Adipocytes, White/metabolism ; Adipose Tissue, Brown/cytology ; Animals ; COS Cells ; *Cell Differentiation/genetics ; Cell Line ; Cercopithecus aethiops ; DNA-Binding Proteins/genetics/*metabolism ; *Gene Expression Regulation, Developmental ; Male ; Mice ; Muscle Development/genetics ; Muscle, Skeletal/cytology/growth & development/*metabolism ; Myogenic Regulatory Factor 5/genetics ; PPAR gamma/genetics ; Transcription Factors/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 2
    ISSN: 1432-1777
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract We have determined the order of a number of SSR and SSC polymorphic markers that map to distal mouse Chromosome (Chr) 4 and have used analysis of these markers in backcrosses designed to test the localization of the curly-tail (ct) mutation. We have confirmed that ct maps to this region, close to the locus D4Mit69. Our results also support the hypothesis that ct is a semidominant, rather than a recessive, mutation, since we have identified abnormal-tailed mice that are likely to be heterozygous at the ct locus. Finally, we examined Pax7 as a candidate gene for the ct mutation and found no evidence of protein sequence differences in ct compared with wild-type mice.
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 3
    Publication Date: 2013-09-25
    Description: Human cortical malformations, including lissencephaly, polymicrogyria and other diseases of neurodevelopment, have been associated with mutations in microtubule subunits and microtubule-associated proteins. Here we report our cloning of the brain dimple ( brdp ) mouse mutation, which we recovered from an ENU screen for recessive perinatal phenotypes affecting neurodevelopment. We identify the causal mutation in the tubulin, beta-2b ( Tubb2b) gene as a missense mutation at a highly conserved residue (N247S). Brdp/brdp homozygous mutants have significant thinning of the cortical epithelium, which is markedly more severe in the caudo-lateral portion of the telencephalon, and do not survive past birth. The cortical defects are largely due to a major increase in apoptosis and we note abnormal proliferation of the basal progenitors. Adult brdp/+ mice are viable and fertile but exhibit behavioral phenotypes. This allele of Tubb2b represents the most severely affected mouse tubulin phenotype reported to date and this is the first report of a tubulin mutation affecting neuronal proliferation and survival.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 4
    Publication Date: 2016-08-10
    Description: We have previously described a forward genetic screen in mice for abnormalities of brain development. Characterization of two hydrocephalus mutants by whole-exome sequencing after whole-genome SNP mapping revealed novel recessive mutations in Dnaaf1 and Lrrc48 . Mouse mutants of these two genes have not been previously reported. The Dnaaf1 mutant carries a mutation at the splice donor site of exon 4, which results in abnormal transcripts. The Lrrc48 mutation is a missense mutation at a highly conserved leucine residue, which is also associated with a decrease in Lrrc48 transcription. Both Dnaaf1 and Lrrc48 belong to a leucine-rich repeat-containing protein family and are components of the ciliary axoneme. Their Chlamydomonas orthologs are known to be required for normal ciliary beat frequency or flagellar waveform, respectively. Some Dnaaf1 or Lrrc48 homozygote mutants displayed laterality defects, suggesting a motile cilia defect in the embryonic node. Mucus accumulation and neutrophil infiltration in the maxillary sinuses suggested sinusitis. Dnaaf1 mutants showed postnatal lethality, and none survived to weaning age. Lrrc48 mutants survive to adulthood, but had male infertility. ARL13B immunostaining showed the presence of motile cilia in the mutants, and the distal distribution of DNAH9 in the axoneme of upper airway motile cilia appeared normal. The phenotypic abnormalities suggest that mutations in Dnaaf1 and Lrrc48 cause defects in motile cilia function.
    Electronic ISSN: 2160-1836
    Topics: Biology
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 5
    Publication Date: 2011-08-03
    Description: There is a wide variation among humans and mice in airway hyperresponsiveness (AHR) in the absence of allergen sensitization, i.e., naïve AHR. Because mast cell (MC) activation is thought to mediate AHR in atopic asthmatic subjects, we asked whether MCs mediate naïve AHR in A/J mice. We generated an A/J congenic strain lacking c-Kit by introgression of the Wv mutation, which resulted in the elimination of MCs and the abrogation of naïve AHR. Imatinib, which disrupts Kit signaling, also abrogated AHR in A/J mice. Remarkably, introduction of the Vga9 Mitf mutation into the A/J background resulted in the ablation of MCs but did not ameliorate AHR. These results indicate that c-Kit is required for development of AHR in an MC-independent fashion.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 6
    Publication Date: 2018-02-09
    Description: Positional cloning of ENU-induced mutations has traditionally relied on analysis of polymorphic variation between two strains. In contrast, the application of whole-genome sequencing (WGS) has enabled gene discovery in mutant lines maintained on an inbred genetic background. This approach utilizes genetic variation derived from ENU-induced variants for mapping and reduces the likelihood of phenotypic variation, making it an ideal method for genetic modifier screening. Here, we describe the results of such a screen, wherein we determined the minimal number of mutant genomic DNA samples to include in our analyses and improved the sensitivity of our screen by individually barcoding each genomic DNA library. We present several unique cases to illustrate this approach’s efficacy, including the discovery of two distinct mutations that generate essentially identical mutant phenotypes, the ascertainment of a non-ENU-induced candidate variant through homozygosity mapping, and an approach for the identification of putative dominant genetic modifiers.
    Electronic ISSN: 2160-1836
    Topics: Biology
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...