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Validated All-in-One™ qPCR Primer for ID1(NM_002165.3) Search again
Product ID:
HQP100610
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ID, bHLHb24
Gene Description:
inhibitor of DNA binding 1
Target Gene Accession:
NM_002165.3(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 is a helix-loop-helix (HLH) protein that can form heterodimers with members of the basic HLH family of transcription factors. The encoded protein has no DNA binding activity and therefore can inhibit the DNA binding and transcriptional activation ability of basic HLH proteins with which it interacts. This protein may play a role in cell growth, senescence, and differentiation. Two transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq].
Gene References into function
- Id1, a dominant negative inhibitor of basic helix-loop-helix proteins, is a direct target gene for BMP
- Id-1 expression is linked with the loss of NF-1/Rb/HDAC-1 transcription repressor complex in metastatic breast cancer
- role in stimulating serum-independent prostate cancer cell proliferation through inactivation of p16(INK4a)/pRB pathway
- TGF beta 1 may be one of the upstream regulators of Id-1
- immunohistochemical studies on NPC samples showed that expression of Id-1 was present in NPC cells but absent in normal tissues. This study demonstrates that Id-1 plays an important role in cell proliferation in NPC cells
- Data suggest that signalling of BMP-2 to stimulate the expression of Id1 would be transduced by BMPR-IA and mediated by Smad1 and Smad4.
- Level of protein expression correlates with poor differentiation, enhanced malignant potential, and more aggressive clinical behavior of epithelial ovarian tumors.
- expression in human endothelial cells induced by Kaposi sarcoma-associated herpesvirus LANA protein, expression in Kaposi sarcoma tumor cells and in vivo
- expression may relate to the metastatic behaviour in human oral squamous cell carcinoma
- dysregulated Id-1 may not only contribute to delaying the senescence program in keratinocytes, it may also contribute to the escape of the relatively undifferentiated tumor cells in BCC from immune surveillance.
- Our results strongly suggest that Id-1 may be one of the upstream regulators of NF-kappaB and activation of NF-kappaB signalling pathway may be essential for Id-1 induced cell proliferation through protection against apoptosis.
- Significantly overexpressed in papillary thyroid cancer. Primarily localized to cytoplasm of thyroid follicular cells. Activation of the mitogen intracellular protein kinase A and protein kinase C signaling pathways up-regulated Id-1 mRNA expression.
- over-expression of Id-1 induces cell proliferation in HCC through inactivation of p16INK4a/retinoblastoma pathway
- Expression of Id-1 was able to reduce androgen-stimulated growth and S phase fraction of the cell cycle in prostatic cancer cells.
- Id1 protein is involved in the process of differentiation of keratinocytes seeen in normal skin and Id1 pathway is activated in psoriasis.
- Id-1 may be an upstream regulator of the Raf/MEK signalling pathway, which plays an essential role in protection against taxol-induced apoptosis
- ID1 may contribute to oncogenesis not only by inhibiting transcriptional activity of basic helix-loop-helix transcription factors and abrogate differentiation but also by subverting centrosome duplication.
- ID-1 expression significantly associated with intratumoral microvessel density in pancreatic cancer
- Id-1 and Id-2 proteins control prostate cancer cell phenotypes and could serve as molecular markers of aggressive human prostate cancer.
- Id1 induction by LMP1 depends on its NF-kappaB activation domain at the COOH-terminal region, CTAR1 and CTAR2. This may facilitate clonal expansion of premalignant nasopharyngeal epithelial cells infected with EBV & promote malignant transformation.
- silencing Id1 expression in young cells by RNA interference induced an increased p16(INK4a) level and premature cellular senescence
- MyoD modulates the rate of Id1 degradation and suggest a dynamic interplay of these factors
- induction of Id1 not only blocks transcriptional activity but also induces myogenin degradation by blocking formation of myogenin-E47 protein complexes.
- Id1 can be up-regulated and p53 down-regulated by a statin in endothelial cells. Regulation of these proteins in endothelial cells may account for the proangiogenic effect of statins.
- Id1 has cell cycle regulatory functions that are similar to those of c-Myc.
- Overexpression of Id1 enhances expression of ICAM-1 and E-selectin, and induces angiogenic processes such as transmigration, matrix metalloproteinase-2 and -9 expression, and tube formation in cultured vascular endothelial cells.
- Idl protein may play an important role in the process of gastric carcinogenesis, and high-level Id I expression may be related to the malignant potential of tumor cells
- Id1 is overexpressed in hyperplastic and neoplastic thyroid tissue and directly regulates the growth of thyroid cancer cells of follicular cell origin, but is not a marker of aggressive phenotype in differentiated thyroid cancer.
- 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
- Thus, we speculate that the regulation of cell growth mediated by CASK may be involved in Id1.
- constitutive expression of Id1 inhibits eosinophil development, whereas in contrast neutrophil differentiation was modestly enhanced
- 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
- In mature human B cells, BMP-6 inhibited cell growth, and rapidly induced an upregulation of Id1.
- Downregulation of Id-1 may be a novel target to inhibit the growth of metastatic cancers through the suppression of angiogenesis.
- Furthermore, by using DCs derived from Id1(-/-) mice that are defective in Flt-1 signaling, we demonstrated that the inhibitory function of VEGF on DC function is most likely mediated by Flt-1.
- degradation is modulated by E12 and E47
- Id1 gene expression may be associated with thyroid cancer cell growth and differentiation.
- Expression of Id1 in HM was significantly higher than that in normal placenta.
- Id-1 protein may be regulated by TNFalpha through the ubiquitin/proteasome degradation pathway and the stability of the Id-1 protein appears to correlate with the sensitivity of TNFalpha-induced apoptosis
- study supports a significant role of the ID1 protein in melanoma progression and patient prognosis; inverse relation between ID1 and TSP-1 expression support an important role of ID1 in regulation of this complex multitarget protein.
- Id1, 3 double-knockdown significantly impaired the ability of gastric cancer cells to form peritoneal metastasis
- results indicate that increased Id-1 expression in prostate cancer cells may play a protective role against apoptosis, and downregulation of Id-1 may be a potential target to increase sensitivity of taxol-induced apoptosis in prostate cancer cells
- Id-1 overexpression is associated with breast tumor angiogenesis
- Study provides evidence for the first time that Id-1 plays a role in both proliferation and survival of esophageal cancer cells.
- Up-regulation of Id-1 was associated with increased EGFR expression, clinical staging and the invasion ability of bladder cancer cells, and inactivation of Id-1 may be a potential therapeutic target to inhibit the invasion by bladder cancer cells.
- The IGFBP3, hRas, JunB, Egr-1, Id1 and MIDA1 genes were up-regulated in psoriatic involved skin compared with uninvolved skin.
- 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
- Interferon-alpha downregulates ID1 ID in cultured human vascular endothelial cells
- Expression of ID1 decreased significantly in chondrocytes while the opposite was seen in mesenchymal stem cells.
- expression of ATF-3 in hypoxic cells represses Id-1 and prevents their loss
- Id-1 is a novel angiogenic factor for HCC metastasis and down-regulation of Id-1 may be a novel target to inhibit HCC metastasis through suppression of angiogenesis.
- Id1 transcriptional inhibitor is a crucial player in mediating cell dedifferentiation of renal tubular epithelium and suggest that epithelial-to-mesenchymal transition is a multistep process.
- In conclusion, we provide the molecular mechanism of the cross talk between HIF-1alpha and Id-1, which may play a critical role in tumor angiogenesis.
- PLZF upregulates apoptosis-inducer TP53INP1, ID1, and ID3 genes, and downregulates the apoptosis-inhibitor TERT gene
- Id1 expression is primarily regulated at the transcriptional level in radial growth phase melanomas and expect that therapies that target Id1 gene expression may be useful in the treatment of Id-associated malignancies.
- significantly enhanced expression of Id-1 has been detected in malignant prostate cell lines and in primary carcinomas; the increase in Id-1 expression was significantly associated with the increasing Gleason score of carcinomas
- caveolin-1 is a novel Id-1 binding partner that mediates the function of Id-1 in promoting prostate cancer progression through activation of the Akt pathway leading to cancer cell invasion and resistance to anticancer drug-induced apoptosis
- Dysregulates centrosome homeostasis at least in part by interfering with S5A/Rpn10 activities at the centrosome.
- a novel tumorigenic role of Id-1 through reorganization of actin cytoskeleton and disassembly of cell-cell adhesion in response to TGF-beta1 in human prostate epithelial cells
- The Id-1 may promote distant metastasis in oesophageal squamous cell carcinoma(ESCC), and both Id-1 may be used for prognostication for ESCC patients.
- These data demonstrate that BMP-6 promotes migration and invasion of prostate cancer cells, potentially through activation of Id-1 and MMP activation.
- Id-1 regulates Bcl-2 and Bax expression through p53 and NF-kappaB in MCF-7 breast cancer cells
- Id-1 overexpression plays an important role in colorectal cancer progression.
- Id1 may contribute to the malignant conversion of primary human melanocytes through extension of cellular lifespan.
- The association of Id1 and Cdh1 is dependent on the canonical destruction box motif of Id1, the increased binding of which may compete with the interaction between Cdh1 and Aurora A, leading to stabilization of Aurora A in Id1-overexpressing cells.
- a novel function of Id-1 in promoting chromosomal instability through modification of APC/C activity during mitosis and provide a novel molecular mechanism accounted for the function of Id-1 as an oncogene.
- Id1 may contribute to early breast cancer by promoting excessive proliferation through cyclin D1.
- The integration of signals at the level of Id gene expression may contribute to the pathogenesis of familial pulmonary arterial hypertension.
- ID1 is an effector of the p53-dependent DNA damage response pathway.
- Id1 is an important target of constitutively activated tyrosine kinases and may be a therapeutic target for leukemias associated with oncogenic tyrosine kinases.
- Id1 inhibited DNA binding by Dril1, and the two proteins co-localized in vitro and in vivo, providing a potential mechanism for suppression of fibrosis by Id1 through inhibition of the profibrotic function of Dril1.
- study reports that the expression of the E6 onco-protein of the high-risk human papillomaviruses is correlated with Id-1 overexpression in the majority of invasive breast cancer tissue samples studied
- These results demonstrated a novel function of Id-1 in regulating HBX protein stability through interaction with the proteasome.
- PGE(2) via EP(4) activates the EGFR --> ERK1/2 --> Egr-1 pathway, leading to increased Id-1 transcription and cell invasion
- both ATF3 and Smad were crucially and synergistically involved in down-regulation of Id-1, which regulated JNK phosphorylation in REIC/Dkk-3-induced apoptosis.
- In uterine cervical cancer, ID-1 might work on tumour advancement through angiogenic activity. ID-1 expression correlated with microvessel counts and with histoscore.
- Id-1, took part in development and progression of colorectal carcinomas and that Id-1 was associated with regulations of EGFR and VEGF.
- Id1 can be strongly up-regulated by Transforming Growth Factor beta1 in the human mammary gland epithelial cell line MCF10A.