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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 08 Dec 2016.

Inhibitor of DNA binding 3, dominant negative helix-loop-helix protein

Id3
The protein encoded by this gene is a helix-loop-helix (HLH) protein that can form heterodimers with other HLH proteins. However, the encoded protein lacks a basic DNA-binding domain and therefore inhibits the DNA binding of any HLH protein with which it interacts. [provided by RefSeq, Aug 2011] (from NCBI)
Top mentioned proteins: Id1, Id2, CAN, HAD, SET
Papers on Id3
Osteogenic potential of human adipose-tissue derived mesenchymal stromal cells cultured on 3D-printed porous structured titanium.
New
van Wijnen et al., Rochester, United States. In Gene, Feb 2016
Compared to standard tissue culture plastic, AMSCs grown in the porous titanium microenvironment showed differences in temporal expression for genes involved in cell cycle progression (CCNB2, HIST2H4), extracellular matrix production (COL1A1, COL3A1), mesenchymal lineage identity (ACTA2, CD248, CD44), osteoblastic transcription factors (DLX3, DLX5, ID3) and epigenetic regulators (EZH1, EZH2).
Clonality Analysis of Immunoglobulin Gene Rearrangement by Next-Generation Sequencing in Endemic Burkitt Lymphoma Suggests Antigen Drive Activation of BCR as Opposed to Sporadic Burkitt Lymphoma.
New
Bellan et al., Siena, Italy. In Am J Clin Pathol, Jan 2016
OBJECTIVES: Recent studies using next-generation sequencing (NGS) analysis disclosed the importance of the intrinsic activation of the B-cell receptor (BCR) pathway in the pathogenesis of sporadic Burkitt lymphoma (sBL) due to mutations of TCF3/ID3 genes.
NKG2D and CD28 receptors differentially activate mTOR to alter murine effector CD8(+) T cell differentiation.
New
Barber et al., United States. In Immunology, Jan 2016
Strong mTORc1 activation in CD28-costimulated cells also increased expression of transcription factors that support effector cell differentiation, namely T-bet, BLIMP1, IRF4, and ID2 whereas low levels of mTORc1 activation allowed for the expression of Eomes, BCL6, and ID3 during NKG2D stimulation, and increased expression of memory markers CD62L and CD127.
Identification of gene expression signature for cigarette smoke exposure response-from man to mouse.
New
Peitsch et al., Neuchâtel, Switzerland. In Hum Exp Toxicol, Dec 2015
The signature consisted of LRRN3, SASH1, PALLD, RGL1, TNFRSF17, CDKN1C, IGJ, RRM2, ID3, SERPING1, and FUCA1.
DNA methylome analysis in Burkitt and follicular lymphomas identifies differentially methylated regions linked to somatic mutation and transcriptional control.
New
Impact
Radlwimmer et al., Leipzig, Germany. In Nat Genet, Nov 2015
Integrative pathway analyses of regions differentially methylated in Burkitt and follicular lymphomas implicated DNA methylation as cooperating with somatic mutation of sphingosine phosphate signaling, as well as the TCF3-ID3 and SWI/SNF complexes, in a large fraction of Burkitt lymphomas.
Induced Developmental Arrest of Early Hematopoietic Progenitors Leads to the Generation of Leukocyte Stem Cells.
New
Kawamoto et al., Yokohama, Japan. In Stem Cell Reports, Nov 2015
By overexpression of the transcriptional inhibitor ID3 in murine hematopoietic progenitor cells and cultivation under B cell induction conditions, the cells undergo developmental arrest and enter a self-renewal cycle.
Inhibitor of differentiation 4 (ID4): From development to cancer.
Review
Chaudhary et al., Atlanta, United States. In Biochim Biophys Acta, 2015
Indeed, numerous studies indicate an oncogenic function for ID1, ID2 and ID3.
The potential role of inhibitor of differentiation-3 in human adipose tissue remodeling and metabolic health.
Review
Vestergaard et al., Copenhagen, Denmark. In Mol Genet Metab, 2014
We aimed to review the literature of the inhibitor of differentiation-3 (ID3) gene in relation to adipose tissue and angiogenesis in humans in order to determine whether ID3 could be involved in the regulation of adipose tissue expansion and metabolic health in human obesity.
New clues to the molecular pathogenesis of Burkitt lymphoma revealed through next-generation sequencing.
Review
Dave et al., Durham, United States. In Curr Opin Hematol, 2014
RECENT FINDINGS: Next-generation sequencing of Burkitt lymphoma has identified recurrent silencing mutations in ID3, a novel tumor suppressor gene.
Oncogenic mechanisms in Burkitt lymphoma.
Review
Staudt et al., Bethesda, United States. In Cold Spring Harb Perspect Med, 2014
TCF-3 is rendered constitutively active in Burkitt lymphoma by two related mechanisms: (1) somatic mutations that inactivate its negative regulator ID3, and (2) somatic mutations in TCF-3 that block the ability of ID3 to bind and interfere with its activity as a transcription factor.
Developments in Burkitt's lymphoma: novel cooperations in oncogenic MYC signaling.
Review
Inman et al., Dundee, United Kingdom. In Cancer Manag Res, 2013
Recurrent mutations in ID3 or TCF3 (E2A) that promote signaling through PI3-kinase have recently been identified in human BL samples, and new therapeutic strategies based on coordinately targeting both the prosurvival factor, B-cell lymphoma-XL, and the PI3-kinase/AKT/mammalian target of rapamycin (mTOR) signaling pathway to synergistically induced BL apoptosis have been proposed.
Antithyroid drugs and their analogues: synthesis, structure, and mechanism of action.
Impact
Mugesh et al., Bengaluru, India. In Acc Chem Res, 2013
The type 3 deiodinase (ID-3) catalyzes the deactivation of thyroid hormone in a process that removes iodine selectively from the tyrosyl ring of T4 to produce 3,3',5'-triiodothyronine (rT3).
New pathogenic mechanisms in Burkitt lymphoma.
Impact
Campo, Barcelona, Spain. In Nat Genet, 2012
Two studies in this issue identify the landscape of somatic mutations in Burkitt lymphoma and highlight the pathogenic and clinical relevance of inactivating mutations of ID3, an inhibitor of the TCF3 transcription factor.
Recurrent mutation of the ID3 gene in Burkitt lymphoma identified by integrated genome, exome and transcriptome sequencing.
Impact
ICGC MMML-Seq Project et al., Kiel, Germany. In Nat Genet, 2012
One of these genes, ID3, mapped to a region of focal homozygous loss in Burkitt lymphoma.
The genetic landscape of mutations in Burkitt lymphoma.
Impact
Dave et al., Durham, United States. In Nat Genet, 2012
We identified 70 genes that were recurrently mutated in Burkitt lymphomas, including ID3, GNA13, RET, PIK3R1 and the SWI/SNF genes ARID1A and SMARCA4.
Loss of E protein transcription factors E2A and HEB delays memory-precursor formation during the CD8+ T-cell immune response.
GeneRIF
Goldrath et al., San Diego, United States. In Eur J Immunol, 2012
These data suggest a model whereby E protein transcription factor activity favors rapid memory-precursor T-cell formation while their negative regulators, Id2 and Id3, are both required for robust effector CD8(+) T-cell response during infection.
ID1 and ID3 regulate the self-renewal capacity of human colon cancer-initiating cells through p21.
Impact
GeneRIF
Dick et al., Toronto, Canada. In Cancer Cell, 2012
Data show that regulation of p21 by ID1 and ID3 is a central mechanism preventing the accumulation of excess DNA damage and subsequent functional exhaustion of cancer-initiating cells (C-ICs).
Wnt/β-catenin signaling changes C2C12 myoblast proliferation and differentiation by inducing Id3 expression.
GeneRIF
ten Dijke et al., Leiden, Netherlands. In Biochem Biophys Res Commun, 2012
These results suggest that Id3 is an important Wnt/beta-catenin induced gene in myoblast cell fate determination.
Inhibitor of differentiation-3 mediates high fat diet-induced visceral fat expansion.
GeneRIF
McNamara et al., Charlottesville, United States. In Arterioscler Thromb Vasc Biol, 2012
Id3 is an important regulator of high-fat diet-induced visceral adipose VEGFA expression, microvascular blood volume, and depot expansion.
Overexpression of Id3 induces apoptosis of A549 human lung adenocarcinoma cells.
GeneRIF
Luo et al., Nanjing, China. In Cell Prolif, 2012
Overexpression of Id3 triggered apoptosis in A549 lung adenocarcinoma cells, implicating Id3 in negative control of tumor growth.
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