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Results describe the expression pattern of Xenopus islet-1 (Xisl-1) in the context of cardiovascular development.
Knock-down of Xisl-1 by specific morpholino leads to severe developmental defects, including eye and heart failure.
This study firstly implicates ISL1 loss-of-function mutation with CHD in humans, which provides novel insight into the molecular mechanism of CHD, implying potential implications for genetic counseling and individually tailored treatment of CHD patients.
The present study revealed that (ISL1) was significantly upregulated in Triplenegative breast cancer (TNBC) tissues in comparison with adjacent normal tissues. Overexpression of ISL1 markedly promoted the proliferation and invasion of the TNBC MDAMB231 and MDAMB468 cell lines, while knockdown of ISL1 inhibited cell invasion and proliferation in these cell lines.
Overexpression of ISL1 in transplanted human mesenchymal stem promotes cell survival in a rat model of myocardial infarction and enhances their paracrine function to protect cardiomyocytes.
ISL1 is a major susceptibility gene for bladder exstrophy and a regulator of urinary tract development.
Mechanistic analyses integrate this unrecognized anti-atrial function of ISL1 with known and newly identified atrial inducers. In this revised view, ISL1 is antagonized by retinoic acid signaling via a novel player, MEIS2.
In the present study, the protein inhibitor of activated STAT Y (PIASy) was identified as a novel Isl1-interacting protein. Furthermore, PIASy and Isl1 upregulate insulin gene expression and insulin secretion in a dose-dependent manner by activating the insulin promoter.
Data show that Islet-1 (ISL1) activated the expression of cyclin B1 (CCNB1), cyclin B2 (CCNB2) and c-myc (c-MYC) genes by binding to the conserved binding sites on their promoters or enhancers.
results identify Isl1 as a crucial transcription factor that plays essential roles in the gene regulatory program directing development of multiple arcuate neuronal subpopulations.
ISL-1 is widely expressed in Olfactory neuroblastoma tumors with neuroendocrine differentiation and therefore of limited value in their differential diagnosis
Data indicate that cells cultured on cardiac muscle laminin (LN)-based substrata in combination with stimulation of the canonical Wnt/beta-catenin pathway showed increased gene expression of ISL1, OCT4, KDR and NKX2.5.
In bladder exstrophy there is a clear correlation with the a mutation of the chromosome 5 ISL1 (5q11.1) gene.
SSBP3 Interacts With Islet-1 and Ldb1 to Impact Pancreatic beta-Cell Target Genes
Concurrent ISL1/HOXA9 methylation in HG-NMIBC reliably predicted tumour recurrence and progression within one year (Positive Predictive Value 91.7%), and was associated with disease-specific mortality
Isl1 overexpression in embryonic stem cells results in normal electrophysiologically functioning cells.
The present study identified the first genome-wide significant locus for classic bladder exstrophy at chromosomal region 5q11.1, and provides strong evidence for the hypothesis that ISL1 is the responsible candidate gene in this region.
Suggest that ISL-1 may be a useful prognostic biomarker and may represent a novel therapeutic target for gastric adenocarcinoma.
Tcf7l2 is regulating proinsulin expression directly via Isl1, Ins1 and indirectly via MafA, NeuroD1 and Pdx1.
ISL-1 is tightly linked to non-Hodgkin lymphoma proliferation and development by promoting c-Myc transcription, and its aberrant expression was regulated by p-STAT3/p-c-Jun/ISL-1 complex activation.
Overexpression of ISL1 in human mesnchymal stem cells promotes angiogenesis in vitro and in vivo through increasing secretion of MCP3 and other paracrine factors.
ISL1 is commonly expressed in rhabdomyosarcoma, particularly the alveolar subtype
Study identified 51 key reprogramming transcription factors that may increase the efficiency and completion of the regeneration process and confirmed that Isl1 in transgenic mice promotes Atoh1-mediated sensory regeneration as a co-reprogramming factor.
Studies demonstrate that Isl1 plays a critical role during development of the external genitalia and forms the basis for a greater understanding of the molecular mechanisms underlying the pathogenesis of BEEC and urinary tract defects in humans.
Mouse cardiac progenitor cells fate transitions are associated with distinct open chromatin states critically depending on Isl1 and Nkx2-5 expression.
ISL1 plays a central role in proper patterning of stem cell-derived enamel in the incisor and indicate that this factor is an important upstream regulator of signaling pathways during tooth development and renewal.
Both ISL1-LHX3 and ISL1-LHX4 bound to the Slit2 enhancer.
results support a model in which Gata6 contributes to repression of Isl1 expression in the anterior of nascent hindlimb buds.
The results demonstrated that Islet1 upregulated expression of general control of amino acid biosynthesis protein 5 (Gcn5) and enhanced the binding of Gcn5 to the promoters of GATA binding protein 4 (GATA4) and NK2 homeobox 5 (Nkx2.5). In addition, Islet-1 downregulated DNA methyltransferase (DNMT)1 expression and reduced its binding to the GATA4 promoter.
Isl1beta is a key additional transcriptional factor for advancing the generation of insulin-producing cells in the liver in combination with PDA (Pdx1, Neurod1, and Mafa).
Overexpression of Islet1 affects the development and function of the cerebello-vestibular system, resulting in hyperactivity.
Results show that specific genomic loci associated with Islet-1 (Isl1) , LIM-homeobox 3 (Lhx3), and LMO4 genes recruit the Isl1-Lhx3 complex to activate the transcription of Isl1, Lhx3, and Lmo4.
these results uncover a novel role for VEGF in controlling proper allocation of Isl1(+) cardiac progenitors to their respective descending lineages
CITED2 and ISL1 proteins interact physically and cooperate to promote embryonic stem cell differentiation toward cardiomyocytes.
Together, the authors show the antagonistic regulation of the alpha-enhancer activity by Pax6 and the LIM protein complex is necessary for the establishment of an inner retinal circuitry, which controls visual adaptation.
PDX1 and ISL1 regulation of insulin gene expression in pancreatic beta cells, was investigated.
Expression of motor neuron effector genes is maintained by transient enhancers bound by Isl1/Lhx3 in nascent motor neurons and Isl1/Onecut1 in maturing hypaxial motor neurons.
These data reveal functional roles for an ISLET1-dependent network integrating beta-catenin/SHH signals in mesenchymal cell survival and outgrowth of the mandible during development.
ISL1 and JMJD3 partner to alter the cardiac epigenome, instructing gene expression changes that drive cardiac differentiation.
Pax2-regulated ISL1 overexpression increases the embryonic ISL1(+) domain and induces accelerated nerve fiber extension and branching in E12.5 embryos.
Nkx2-5 and nkx2.7 genes restrict proliferation of heart field progenitors in the outflow tract, delimit the number of progenitors at the venous pole and pattern the sinoatrial node acting through Isl1 repression.
Arx contributes to patterning in the prethalamic region, while Isl1 is required for differentiation of prethalamic dopaminergic neurons.
Ajuba plays a central role in regulating the second heart field during heart development by linking retinoic acid signaling to the function of Isl1, a key transcription factor in cardiac progenitor cells.
Isl1 is required for the selective outgrowth of the peripheral axons of Rohon-beard neurons.
prdm1a Regulates sox10 and islet1 in the development of neural crest and Rohon-Beard sensory neurons.
By direct comparison of the upstream flanking regions of the zebrafish and human isl1 genes, we identified another highly conserved noncoding element.
primary motoneuron subtypes are likely to be specified by factors that act in parallel to or upstream of islet1 and islet2
Nkx6 proteins regulate MiP motorneuron development at least in part by maintaining the islet1 expression that is required both to promote the MiP subtype and to suppress interneuron development.
This gene encodes a member of the LIM/homeodomain family of transcription factors. The encoded protein binds to the enhancer region of the insulin gene, among others, and may play an important role in regulating insulin gene expression. The encoded protein is central to the development of pancreatic cell lineages and may also be required for motor neuron generation. Mutations in this gene have been associated with maturity-onset diabetes of the young.
, ISL1 transcription factor, LIM/homeodomain, (islet-1)
, domesticus (clone 1.7 kB) islet-1
, insulin gene enhancer protein ISL-1
, ISL1 transcription factor, LIM/homeodomain
, ISL1 transcription factor LIM/homeodomain (islet-1)
, ISL1 transcription factor, LIM/homeodomain 1
, isl-1 homeobox
, Insulin gene enhancer protein ISL-1
, Islet 1
, Lim-homeodomain protein Islet1
, insulin related protein
, insulin gene enhancer protein isl-1