scholarly journals Examining the role of SUMOylation in C. elegans T-box transcription factor TBX-2 function

2011 ◽  
Vol 356 (1) ◽  
pp. 261
Author(s):  
Paul Huber ◽  
Tanya Crum ◽  
Peter Okkema
Keyword(s):  
Transcription Factor ◽  
T Box ◽  
C Elegans

scholarly journals Assessing the role of the T-box transcription factor Eomes in B cell differentiation during either Th1 or Th2 cell-biased responses

PLoS ONE ◽  
2018 ◽  
Vol 13 (12) ◽  
pp. e0208343 ◽  
Author(s):  
Lucy Cooper ◽  
Lauren Hailes ◽  
Amania Sheikh ◽  
Colby Zaph ◽  
Gabrielle T. Belz ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cell Differentiation ◽  
B Cell ◽  
B Cell Differentiation ◽  
T Box ◽  
Th2 Cell

scholarly journals Down-regulation of miR-10a-5p promotes proliferation and restricts apoptosis via targeting T-box transcription factor 5 in inflamed synoviocytes

2018 ◽  
Vol 38 (2) ◽  
Author(s):  
Nazim Hussain ◽  
Wenhua Zhu ◽  
Congshan Jiang ◽  
Jing Xu ◽  
Manman Geng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Transcription Factor ◽  
Quantitative Polymerase Chain Reaction ◽  
Cell Counting ◽  
Control Group ◽  
Down Regulation ◽  
T Box ◽  
Proliferation And Apoptosis ◽  
Polymerase Chain

Synoviocytes from rheumatoid arthritis (RA) patients share certain features with tumor cells, such as over proliferation and invasion. Anomalous microRNA (miRNA) expression may participate in the pathogenesis of RA in different ways. The objective of the present study was to observe the role of miR-10a-5p targeting T-box transcription factor 5 (TBX5) gene on synoviocyte proliferation and apoptosis in RA. Human synovial sarcoma cell line, SW982 cells stimulating with interleukin-1β (IL-1β) were transfected with miR-10a-5p mimic and siRNA of TBX5. The real-time quantitative polymerase chain reaction (RT-qPCR) and Western blotting analysis were used to evaluate the expression level of miR-10a-5p and TBX5 in SW982 cells respectively. Further, the proliferation and apoptosis of SW982 cells after treatment were determined by cell counting kit (CCK-8) and flow cytometry analysis respectively. We found that the miR-10a-5p showed down-regulated while TBX5 showed up-regulated expression in synoviocytes after stimulation with IL-1β. The miR-10a-5p mimic treatment showed a decline in cell proliferation while the increased rate of cell apoptosis as compared with control. Moreover, knockdown of TBX5 favored the apoptosis and reduced the cell proliferation as compared with control group. We conclude that down-regulation of miR-10a-5p promotes proliferation and restricts apoptosis via targeting TBX5 in inflamed synoviocytes.

scholarly journals Expression Pattern, Regulation, and Biological Role of Runt Domain Transcription Factor, run, in Caenorhabditis elegans

2002 ◽  
Vol 22 (2) ◽  
pp. 547-554 ◽  
Author(s):  
Seunghee Nam ◽  
Yun-Hye Jin ◽  
Qing-Lin Li ◽  
Kwang-Youl Lee ◽  
Goo-Bo Jeong ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Caenorhabditis Elegans ◽  
Essential Role ◽  
Regulatory Elements ◽  
Intestinal Cells ◽  
Human Leukemia ◽  
Runt Domain ◽  
C Elegans ◽  
Intron Region

ABSTRACT The Caenorhabditis elegans run gene encodes a Runt domain factor. Runx1, Runx2, and Runx3 are the three known mammalian homologs of run. Runx1, which plays an essential role in hematopoiesis, has been identified at the breakpoint of chromosome translocations that are responsible for human leukemia. Runx2 plays an essential role in osteogenesis, and inactivation of one allele of Runx2 is responsible for the human disease cleidocranial dysplasia. To understand the role of run in C. elegans, we used transgenic run::GFP reporter constructs and a double-stranded RNA-mediated interference method. The expression of run was detected as early as the bean stage exclusively in the nuclei of seam hypodermal cells and lasted until the L3 stage. At the larval stage, expression of run was additionally detected in intestinal cells. The regulatory elements responsible for the postembryonic hypodermal seam cells and intestinal cells were separately located within a 7.2-kb-long intron region. This is the first report demonstrating that an intron region is essential for stage-specific and cell type-specific expression of a C. elegans gene. RNA interference analysis targeting the run gene resulted in an early larva-lethal phenotype, with apparent malformation of the hypodermis and intestine. These results suggest that run is involved in the development of a functional hypodermis and gut in C. elegans. The highly conserved role of the Runt domain transcription factor in gut development during evolution from nematodes to mammals is discussed.

scholarly journals Caenorhabditis eleganssensory neurons modulate pathogen specific responses via HLH-30/TFEB transcription factor and FSHR-1 GPCR axes of immunity

2019 ◽  
Author(s):  
Anjali Gupta ◽  
Manoj Varma ◽  
Varsha Singh
Keyword(s):  
Immune Response ◽  
Pattern Recognition ◽  
Transcription Factor ◽  
Sensory Perception ◽  
Immune Effector ◽  
C Elegans ◽  
Classical Pattern ◽  
Molecular Patterns ◽  
Ciliated Neurons

ABSTRACTPattern recognition receptors allow animals to sense microbe associated molecular patterns and mount effective immune responses. It is not clear howCaenorhabditis elegansrecognizes pathogenic microbes in absence of classical pattern recognition pathways. Here, we asked if sensory neurons ofC. elegansallow it to distinguish between pathogens. Exposure ofC. elegansto a Gram positive bacteriumEnterococcus faecalisor to a Gram negative bacteriumPseudomonas aeruginosashowed predominantly pathogen-specific signatures. Using nematodes defective in sensory perception, we show that neuronal sensing is essential to mount pathogen specific immune response. OSM-6 expressing, ciliated neurons exert non-cell autonomous control of immune effector production via an OSM-6-FSHR-1 GPCR axis as well as an OSM-6-HLH-30/TFEB transcription factor axis duringE. faecalisinfection. OSM-6-FSHR-1 axis also controls immune response toP. aeruginosa. In all, this study delineates essential role of sensory perception in the regulation of pathogen-specific immunity inC. elegans.

scholarly journals Role of T-box gene tbx-2 for anterior foregut muscle development in C. elegans

2007 ◽  
Vol 302 (1) ◽  
pp. 25-39 ◽  
Author(s):  
Pliny A. Smith ◽  
Susan E. Mango
Keyword(s):  
Muscle Development ◽  
T Box ◽  
C Elegans

scholarly journals The T-Box Transcription Factor SEA-1 Is an Autosomal Element of the X:A Signal that Determines C. elegans Sex

2005 ◽  
Vol 9 (3) ◽  
pp. 339-349 ◽  
Author(s):  
Jennifer R. Powell ◽  
Margaret M. Jow ◽  
Barbara J. Meyer
Keyword(s):  
Transcription Factor ◽  
T Box ◽  
C Elegans

The C. elegans POU-domain transcription factor UNC-86 regulates the tph-1 tryptophan hydroxylase gene and neurite outgrowth in specific serotonergic neurons

Development ◽  
2002 ◽  
Vol 129 (16) ◽  
pp. 3901-3911 ◽  
Author(s):  
Ji Ying Sze ◽  
Shenyuan Zhang ◽  
Jie Li ◽  
Gary Ruvkun
Keyword(s):  
Transcription Factor ◽  
Neurite Outgrowth ◽  
Serotonin Reuptake ◽  
Tryptophan Hydroxylase ◽  
Serotonin Synthesis ◽  
Serotonergic Neurons ◽  
C Elegans ◽  
Neuronal Types ◽  
Specific Regulation

A fundamental question in developmental neurobiology is how a common neurotransmitter is specified in different neuronal types?. We describe cell-specific regulation of the serotonergic phenotype by the C. elegans POU-transcription factor UNC-86. We show that unc-86 regulates particular aspects of the terminal neuronal identity in four classes of serotonergic neurons, but that the development of the ADF serotonergic neurons is regulated by an UNC-86-independent program. In the NSM neurons, the role of unc-86 is confined in late differentiation; the neurons are generated but do not express genes necessary for serotonergic neurotransmission. unc-86-null mutations affect the expression in NSM of tph-1, which encodes the serotonin synthetic enzyme tryptophan hydroxylase, and cat-1, which encodes a vesicular transporter that loads serotonin into synaptic vesicles, suggesting that unc-86 coordinately regulates serotonin synthesis and packaging. However, unc-86-null mutations do not impair the ability of NSM to reuptake serotonin released from the ADF serotonergic chemosensory neurons and this serotonin reuptake is sensitive to the serotonin reuptake block drugs imipramine and fluoxetine, demonstrating that serotonin synthesis and reuptake is regulated by distinct factors. The NSM neurons in unc-86-null mutants also display abnormal neurite outgrowth, suggesting a role of unc-86 in regulating this process as well.

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