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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Inhibitor of DNA binding 2, dominant negative helix-loop-helix protein

The protein encoded by this gene belongs to the inhibitor of DNA binding family, members of which are transcriptional regulators that contain a helix-loop-helix (HLH) domain but not a basic domain. Members of the inhibitor of DNA binding family inhibit the functions of basic helix-loop-helix transcription factors in a dominant-negative manner by suppressing their heterodimerization partners through the HLH domains. This protein may play a role in negatively regulating cell differentiation. A pseudogene of this gene is located on chromosome 3. [provided by RefSeq, Aug 2011] (from NCBI)
Top mentioned proteins: Id1, Id3, CAN, HAD, V1a
Papers using Id2 antibodies
Does RNA editing play a role in the development of urinary bladder cancer?
Gallo Angela et al., In International Journal of Cancer. Journal International du Cancer, 2008
... (ID1) human heart from Clonthech, BD Biosciences; (ID2) human bladder from Clonthech, BD Biosciences; (ID3) normal blood lymphocytes, ...
The role of receptor internalization in CD95 signaling.
Najbauer Joseph, In PLoS ONE, 2005
... both from Pharmingen; mouse monoclonal anti-Fas (clone CH11) from Upstate Biotechnology; mouse monoclonal anti-MMP7 (clone ID2) from Abcam; mouse monoclonal anti-NF-κB (NLS ...
Papers on Id2
An ID2-dependent mechanism for VHL inactivation in cancer.
Lasorella et al., New York City, United States. In Nature, Feb 2016
The ID2 protein supports cancer hallmarks including the cancer stem cell state.
Hypoxia Promotes Cancer Stem Cells via ID2-Dependent VHL Inactivation.
In Cancer Discov, Feb 2016
UNASSIGNED: Hypoxia inactivates DYRK1, preventing ID2 phosphorylation and promoting CSCs and HIF2α stabilization.
NKG2D and CD28 receptors differentially activate mTOR to alter murine effector CD8(+) T cell differentiation.
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.
Epigenetic role of CCAAT box-binding transcription factor NF-Y on ID gene family in human embryonic carcinoma cells.
Shahhoseini et al., Tehrān, Iran. In Iubmb Life, Nov 2015
The results demonstrated a marked down-regulation of ID1, ID2, and ID3 genes, parallel to a loss of NF-Y binding to the promoters of these genes.
Curcumin alters gene expression-associated DNA damage, cell cycle, cell survival and cell migration and invasion in NCI-H460 human lung cancer cells in vitro.
Chung et al., Yilan, China. In Oncol Rep, Oct 2015
Specifically, the up‑ and downregulated genes included CCNE2, associated with DNA damage; ID3, associated with cell survival and 146 genes with a >2- to 3-fold change including the TP53INP1 gene, associated with DNA damage; CDC6, CDCA5, TAKMIP2, CDK14, CDK5, CDCA76, CDC25A, CDC5L and SKP2, associated with cell cycle; the CARD6, ID1 and ID2 genes, associated with cell survival and the BRMS1L, associated with cell migration and invasion.
Innate Lymphoid Cells Control Early Colonization Resistance against Intestinal Pathogens through ID2-Dependent Regulation of the Microbiota.
Fu et al., Chicago, United States. In Immunity, May 2015
ID2, an essential transcriptional regulator for the development of innate lymphoid cell (ILC) progenitors, remains highly expressed in differentiated ILCs with unknown function.
Inhibitor of differentiation 4 (ID4): From development to cancer.
Chaudhary et al., Atlanta, United States. In Biochim Biophys Acta, 2015
Indeed, numerous studies indicate an oncogenic function for ID1, ID2 and ID3.
High basal Wnt signaling is further induced by PI3K/mTor inhibition but sensitive to cSRC inhibition in mammary carcinoma cell lines with HER2/3 overexpression.
Mol et al., Utrecht, Netherlands. In Bmc Cancer, 2014
RESULTS: High basal Wnt/LEF1 activity was associated with overexpression of HER2/3, ID1, ID2, RAC1 and HSP90 together with low to absent cMET and PTEN mRNA expression, suggesting a connection between Wnt- and HER-signaling pathways.
Genomic analysis of diffuse intrinsic pontine gliomas identifies three molecular subgroups and recurrent activating ACVR1 mutations.
Hawkins et al., Toronto, Canada. In Nat Genet, 2014
Mutations in ACVR1 were constitutively activating, leading to SMAD phosphorylation and increased expression of the downstream activin signaling targets ID1 and ID2.
A committed precursor to innate lymphoid cells.
Bendelac et al., Chicago, United States. In Nature, 2014
PLZF(high) precursors also expressed high amounts of ID2 and GATA3, as well as TOX, a known regulator of PLZF-independent NK and LTi lineages.
Development of human natural killer cells and other innate lymphoid cells.
Mingari et al., Genova, Italy. In Semin Immunol, 2014
In this context, it has been postulated that all ILC share a common precursor expressing the ID2 transcription factor.
Reduced lymphoid lineage priming promotes human hematopoietic stem cell expansion.
Dick et al., Toronto, Canada. In Cell Stem Cell, 2014
Conversely, reducing ID2 expression levels increases lymphoid potential.
The Fanconi anemia ID2 complex: dueling saxes at the crossroads.
Howlett et al., United States. In Cell Cycle, 2013
Fanconi anemia (FA) is a rare recessive genetic disease characterized by congenital abnormalities, bone marrow failure and heightened cancer susceptibility in early adulthood.
Remembering one's ID/E-ntity: E/ID protein regulation of T cell memory.
Goldrath et al., San Diego, United States. In Curr Opin Immunol, 2013
Here, we discuss the role of ID2 and ID3 in promoting the generation and survival of effector and memory populations, particularly highlighting their reciprocal roles in shaping the CD8(+) T cell response unique to the inflammatory milieu.
Transcriptional regulator Id2 is required for the CD4 T cell immune response in the development of experimental autoimmune encephalomyelitis.
Zhuang et al., Durham, United States. In J Immunol, 2012
A critical role of Id2 is revealed in the control of effector CD4 T cell population size and the development of T helper (Th) cell type 17-mediated autoimmune encephalomyelitis.
Loss of E protein transcription factors E2A and HEB delays memory-precursor formation during the CD8+ T-cell immune response.
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.
Overexpressed DNA-binding protein inhibitor 2 as an unfavorable prognosis factor promotes cell proliferation in nasopharyngeal carcinoma.
Fang et al., Guangzhou, China. In Acta Biochim Biophys Sin (shanghai), 2012
ID2 in nucleus was increased in nasopharyngeal carcinoma when compared with that in normal nasopharynx tissues. Higher expression level of nuclear ID2 was significantly associated with tumor size, lymph node metastasis, and clinical stage.
ID2: A negative transcription factor regulating oligodendroglia differentiation.
Yao et al., Chongqing, China. In J Neurosci Res, 2012
This review reported that ID2 protein is a negative transcription factor regulating oligodendroglia differentiation.
Notch, Id2, and RORγt sequentially orchestrate the fetal development of lymphoid tissue inducer cells.
Eberl et al., Paris, France. In J Exp Med, 2012
Both the expression of Id2 and Notch are required for the generation of alpha4beta7(+) RORgammat(-) fetal progenitors, but Notch subsequently blocks progression to the RORgammat(+) stage and final maturation of lymphoid tissue inducer cells
Bmps and id2a act upstream of Twist1 to restrict ectomesenchyme potential of the cranial neural crest.
Crump et al., Los Angeles, United States. In Plos Genet, 2011
the ventral migration of Cranial neural crest cells (CNCCs) away from a source of Bmps in the dorsal ectoderm promotes ectomesenchyme development by relieving Id2a-dependent repression of Twist1 function.
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