Isolation of MYADM, a novel hematopoietic-associated marker gene expressed in multipotent progenitor cells and up-regulated during myeloid differentiation

Pettersson, M; Dannaeus, Karin; Nilsson, Kenneth; Jönsson, Jan‐Ingvar

doi:10.1002/jlb.67.3.423

Cited by 28 publications

(25 citation statements)

References 50 publications

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“…Indeed, HA-tagged MYADM appeared mainly as an integral membrane protein in the nuclear membrane and in intracytoplasmic membrane locations. This is in agreement with the reports suggesting the MYADM gene to encode a protein containing multiple putative transmembrane domains [5,6]. In addition, based on analysis of conserved domain involved in membarne apposition events, it has been proposed that MYADM is a distant member of the MARVEL gene family [31].…”

Section: Discussionsupporting

confidence: 91%

“…The genes for both human and mouse MYADM have been described and show high sequence homology and similar genomic structure [5,6]. In both species the gene is divided into three exons, of which exon 3 contains the complete coding sequence (not shown).…”

Section: Discussionmentioning

confidence: 99%

“…This approach led to the identification of a novel gene that was strongly upregulated during myeloid differentiation, termed MYADM for myeloid-associated differentiation marker gene [5]. Interestingely, MYADM was shown to be expressed exclusively in the myeloid lineage of hematopoietic cells.…”

Section: Introductionmentioning

confidence: 99%

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Characterization of the Mouse Myeloid-associated Differentiation Marker (Myadm) Gene: Promoter Analysis and Protein Localization

2005

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

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Characterization of the Mouse Myeloid-associated Differentiation Marker (Myadm) Gene: Promoter Analysis and Protein Localization

2005

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“…The most significantly downregulated DEGs in these GO terms play a role in immunity (myeloid differentiation marker gene, MYADM, FC of 6 [118] and serpin peptidase inhibitor, SERPIN, FC of 9, an inhibitor of the complement classical pathway [119]), pain (purinergic receptor, P2X3, FC of 7) (120), and cell division (sushi domain-containing 2, SUSD2, FC of 9) (121) (Fig. 11B).…”

Section: Fig 10mentioning

confidence: 99%

Acute Simian Varicella Virus Infection Causes Robust and Sustained Changes in Gene Expression in the Sensory Ganglia

Arnold

Girke

Sureshchandra

et al. 2016

J Virol

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Primary infection with varicella-zoster virus (VZV), a neurotropic alphaherpesvirus, results in varicella. VZV establishes latency in the sensory ganglia and can reactivate later in life to cause herpes zoster. The relationship between VZV and its host during acute infection in the sensory ganglia is not well understood due to limited access to clinical specimens. Intrabronchial inoculation of rhesus macaques with simian varicella virus (SVV) recapitulates the hallmarks of VZV infection in humans. We leveraged this animal model to characterize the host-pathogen interactions in the ganglia during both acute and latent infection by measuring both viral and host transcriptomes on days postinfection (dpi) 3, 7, 10, 14, and 100. SVV DNA and transcripts were detected in sensory ganglia 3 dpi, before the appearance of rash. CD4 and CD8 T cells were also detected in the sensory ganglia 3 dpi. Moreover, lung-resident T cells isolated from the same animals 3 dpi also harbored SVV DNA and transcripts, suggesting that T cells may be responsible for trafficking SVV to the ganglia. Transcriptome sequencing (RNA-Seq) analysis showed that cessation of viral transcription 7 dpi coincides with a robust antiviral innate immune response in the ganglia. Interestingly, a significant number of genes that play a critical role in nervous system development and function remained downregulated into latency. These studies provide novel insights into host-pathogen interactions in the sensory ganglia during acute varicella and demonstrate that SVV infection results in profound and sustained changes in neuronal gene expression. IMPORTANCEMany aspects of VZV infection of sensory ganglia remain poorly understood, due to limited access to human specimens and the fact that VZV is strictly a human virus. Infection of rhesus macaques with simian varicella virus (SVV), a homolog of VZV, provides a robust model of the human disease. Using this model, we show that SVV reaches the ganglia early after infection, most likely by T cells, and that the induction of a robust innate immune response correlates with cessation of virus transcription. We also report significant changes in the expression of genes that play an important role in neuronal function. Importantly, these changes persist long after viral replication ceases. Given the homology between SVV and VZV, and the genetic and physiological similarities between rhesus macaques and humans, our results provide novel insight into the interactions between VZV and its human host and explain some of the neurological consequences of VZV infection. V aricella-zoster virus (VZV) is a neurotropic alphaherpesvirus and the causative agent of varicella (chickenpox) (1). VZV establishes latency in the sensory ganglia and can reactivate later in life to cause herpes zoster (shingles), a painful disease that affects almost 1 million individuals in the United States alone (2). VZV is transmitted through the inhalation of virus-laden saliva droplets or by direct contact with the infectious fluid from vesicles...

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“…17 Lisch7 is a liver-specific transcription factor involved in the regulation of lipid metabolism, which may mediate partitioning of dietary lipid between different tissues. Myadm is upregulated during myeloid differentiation 18 but its exact function is unknown. Fah (fumarylacetoacetate hydrolase) is a nuclear protein that binds to DNA and possesses catalytic, fumarylacetoacetase and hydrolase activities, which are involved in aromatic amino acid family metabolism, phenylalanine catabolism, regulation of transcription, and DNA-dependent tyrosine catabolism.…”

Section: Discussionmentioning

confidence: 99%

Identification of Hypertension-Related Genes Through an Integrated Genomic-Transcriptomic Approach

Yagil

Hübner²,

Monti³

et al. 2005

Circulation Research

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Abstract-In search for the genetic basis of hypertension, we applied an integrated genomic-transcriptomic approach to identify genes involved in the pathogenesis of hypertension in the Sabra rat model of salt-susceptibility. In the genomic arm of the project, we previously detected in male rats two salt-susceptibility QTLs on chromosome 1, SS1a (D1Mgh2-D1Mit11; span 43.1 cM) and SS1b (D1Mit11-D1Mit4; span 18 cM). In the transcriptomic arm, we studied differential gene expression in kidneys of SBH/y and SBN/y rats that had been fed regular diet or salt-loaded. We used the Affymetrix Rat Genome RAE230 GeneChip and probed Ͼ30 000 transcripts. The research algorithm called for an initial genome-wide screen for differentially expressed transcripts between the study groups. This step was followed by cluster analysis based on 2ϫ2 ANOVA to identify transcripts that were of relevance specifically to salt-sensitivity and hypertension and to salt-resistance. The two arms of the project were integrated by identifying those differentially expressed transcripts that showed an allele-specific hypertensive effect on salt-loading and that mapped within the defined boundaries of the salt-susceptibility QTLs on chromosome 1. The differentially expressed transcripts were confirmed by RT-PCR. Of the 2933 genes annotated to rat chromosome 1, 1102 genes were identified within the boundaries of the two blood pressure QTLs. The microarray identified 2470 transcripts that were differentially expressed between the study groups. Cluster analysis identified genome-wide 192 genes that were relevant to salt-susceptibility and/or hypertension, 19 of which mapped to chromosome 1. Eight of these genes mapped within the boundaries of QTLs

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Isolation of MYADM, a novel hematopoietic-associated marker gene expressed in multipotent progenitor cells and up-regulated during myeloid differentiation

Cited by 28 publications

References 50 publications

Characterization of the Mouse Myeloid-associated Differentiation Marker (Myadm) Gene: Promoter Analysis and Protein Localization

Characterization of the Mouse Myeloid-associated Differentiation Marker (Myadm) Gene: Promoter Analysis and Protein Localization

Acute Simian Varicella Virus Infection Causes Robust and Sustained Changes in Gene Expression in the Sensory Ganglia

Identification of Hypertension-Related Genes Through an Integrated Genomic-Transcriptomic Approach

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