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Validated All-in-One™ qPCR Primer for ID2(NM_002166.4) Search again
Product ID:
HQP009273
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
GIG8, ID2A, ID2H, bHLHb26
Gene Description:
inhibitor of DNA binding 2
Target Gene Accession:
NM_002166.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
The protein encoded by this gene belongs to the inhibitor of DNA binding (ID) family, members of which are transcriptional regulators that contain a helix-loop-helix (HLH) domain but not a basic domain. Members of the ID 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 has been identified for this gene. [provided by RefSeq].
Gene References into function
- Id2 is critical for cellular proliferation and is the oncogenic effector of N-myc in human neuroblastoma.
- determination as a novel target of transcriptional activation by EWS-ETS fusion proteins in Ewing family tumors
- upregulation is mediated by the chimeric EWS/ets protein in Ewing sarcoma
- We found no correlation between MYCN and ID2 expression in neuroblastoma cell lines or tumor specimens. However, we did find a significant positive correlation between MYC and ID2 expressions in both MYCN-amplified and single-copy tumor specimens
- Id2 is up-regulated during dendritic cells development in vitro and crucial for the development of distinct dendritic cells subsets in vivo
- Transcriptional regulation of ID2 by the MycN oncoprotein is unlikely to be a seminal molecular event resulting in a highly malignant neuroblastoma phenotype.
- Mad expression and Id2 down-regulation are important events during the TGF-beta cytostatic program in epithelial cells.
- The decreased level of Id2 was associated with growth suppression and does support the prevalent conception of the action of Id2 as a stimulator of cell growth
- ID-2 appears to act as an important protein for the maintenance of a differentiated and noninvasive phenotype in normal and transformed breast cells.
- Id2 developmental regulator degradation is targeted via N-terminal ubiquitination
- Id-1 and Id-2 proteins control prostate cancer cell phenotypes and could serve as molecular markers of aggressive human prostate cancer.
- Hypoxia-induced ID2 expression could play a significant role in the previously observed dedifferentiation of hypoxic neuroblastoma cells, which in a clinical setting could lead to less mature and more aggressive tumors.
- Id1, 2 and 3 might play a role in the early stages of hepatocarcinogenesis, but not in the development of advanced carcinoma, and might consequently be related to HCC dedifferentiation
- reenters the cell cycle after radiation-induced cell cycle arrest to permit the recovery of keratinocytes
- Constitutive Id2 expression accelerates final maturation of both eosinophils and neutrophils, whereas inhibition of Id2 expression blocks differentiation of both lineages
- These results indicate ID1 and ID2 are important retinoic acid responsive genes in acute promyelocytic leukemia [APL], and suggest that inhibition of specific bHLH transcription factor complexes may play a role in the therapeutic effect of ATRA in APL
- PU.1 and Id2 modulate lineage options of langerhans cell precursors, downstream of TGF-beta1.
- PKD2 regulates the cell cycle through direct interaction with Id2; Id2 expression suppresses the induction of a cdk inhibitor, p21, by either PKD1 or PDK2. The PDK2-Id2 interaction is regulated by PDK1-dependent phosphorylation of PDK2.
- enigma homolog enigma-like LIM domain protein is a restraining factor of the oncogenic activity of Id proteins in neural tumors
- ID proteins (ID1, ID2, ID3 and ID4) were significantly increased in Mecp2-deficient Rett syndrome brain; ID genes are ideal targets for MeCP2 regulation of neuronal maturation that may explain the molecular pathogenesis of Rett syndrome
- Global gene expression analysis in neuroblastoma cells engineered to acutely express the E protein E47 and Id2, showed that p57Kip2 is a target of E47.
- findings indicate that deregulated Id activity might be useful to reprogramme quiescent neurons into the axonal growth mode
- ID2, which can inactivate E2A and perhaps PAX5, is not detectable in normal B cells but is strongly and uniformly expressed in Hodgkin-Reed/Sternberg (HRS) cells of all cases of classical Hodgkin's lymphoma (HL).
- OLIG2 expression was predominant over ID2 expression in oligodendroglial tumors, while ID2 expression was predominant over OLIG2 expression in astrocytic tumors.
- RFX1 mediates the immediate early response of the Id2 gene by serum stimulation and suggest that the function of RFX1 is regulated intramolecularly in its suppression in growth-arrested cells.
- Our data demonstrate that IL-1beta-induced Id2 expression in VSMC is mediated by the transcription factor Egr-1 in VSMC.
- The high levels of Id-2 expression in both cytoplasmic and nuclear regions predicted longer patient survival, and Id-2 may be used for prognostication for oesophageal squamous cell carcinoma (ESCC) patients.
- Id2 commonly is overexpressed in highly proliferative T-cell lymphomas, and its expression may result from transcriptional activation of myc in these tumors.
- ID2 plays a significant role in the metastatic process during progression of HCC. This action might be explained, at least in part, by altered cell mobility due to decreased secretion of VEGF.
- The integration of signals at the level of Id gene expression may contribute to the pathogenesis of familial pulmonary arterial hypertension
- activation of protein kinase A elicits an immediate response through induction of genes such as ID2 and FosB, followed by sustained secretion of bone-related cytokines such as BMP-2, IGF-1, and IL-11
- Id2 is upregulated in CRC, and is important in promoting cell survival.
- Results suggest that in lymphoma cells overexpressing growth hormone, there is an upregulation of Id2 protein that appears to involve STAT protein activity.
- This study shows that Id2 is an important regulator of vasculogenic mimicry. Specifically, Id2 affects VE-cadherin expression, and is critical for the formation of vasculogenic-like networks.
- ID2 protein was expressed in 83.3% of this group of classical Hodgkin lymphoma, staining strongly in both cytoplasm and nucleus of the Hodgkin and Reed-Sternberg (HRS) cells, and was positively correlated with EBV-LMP1
- the relationship between the expression of ID2 in non-small cell lung cancer (NSCLC) patients and the clinicopathological features and prognosis of these patients