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Validated All-in-One™ qPCR Primer for HOXA9(NM_152739.3) Search again
Product ID:
HQP008980
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ABD-B, HOX1, HOX1.7, HOX1G
Gene Description:
homeobox A9
Target Gene Accession:
NM_152739.3(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.
Summary
In vertebrates, the genes encoding the class of transcription factors called homeobox genes are found in clusters named A, B, C, and D on four separate chromosomes. Expression of these proteins is spatially and temporally regulated during embryonic development. This gene is part of the A cluster on chromosome 7 and encodes a DNA-binding transcription factor which may regulate gene expression, morphogenesis, and differentiation.
Gene References into function
- demonstrates a physiological role of the mouse protein in blood cell differentiation, with the greatest apparent influence at the level of the commited progenitor
- the fusion gene NUP98-HOXA9 is an important gene in myeloid leukemogenesis.
- Nup98-HoxA9 immortalizes myeloid progenitors, enforces expression of Hoxa9, Hoxa7 and Meis1, and alters cytokine-specific responses in a manner similar to that induced by retroviral co-expression of Hoxa9 and Meis1.
- The HOXA9 cluster gene is frequently expressed in cell lines from acute myeloid leukemia cases with 11p15 translocations; in some cases HOX9 is not fused to NUP98.
- The NUP98/HOXA9 FUSION transcript was detected by PC at exon A and not exon B of NUP98.
- HOXA9 complexed with Pbx1 and DNA, so that the posterior Hox hexapeptide adopts an altered conformation.
- Nup98-HOXA9 has a role in inducing gene transcription in myeloid cells
- B-lineage development can proceed in t(4;11) leukemic blasts in the absence of HOX-A gene expression.
- Hoxa9 and Hoxa7 as well as the Hox coregulators Meis1 and Pbx3 among the targets upregulated by MLL-ENL-ERtm in conditionally transformed cells
- Lower expression of HOXA9 is associated with acute myeloid leukemia-M2
- HoxA9 binds to the EphB4 promoter & stimulates its expression resulting in an increase of endothelial cell migration and tube forming activity. Thus, modulation of EphB4 expression may contribute to the proangiogenic effect of HoxA9 in endothelial cells.
- suggest that MLL aberrations may regulate MEIS1 and HOXA9 gene expression in ALL-derived cell lines, while AML-derived cell lines express these genes independently of the MLL status
- HOXA9 nuclear transport is induced by thrombopoietin in immature hematopoietic cells
- Dnalc4, Fcgr2b, Fcrl, and Con1 genes cooperated with NUP98-HOXA9 in transforming NIH 3T3 cells
- advantage to Meis1-HoxA9 coexpressing cells in vivo, leading to leukemogenesis.
- HOXA9, is a positive regulator of eIF4E. HOXA9 stimulates eIF4E-dependent export of cyclin D1 and ornithine decarboxylase (ODC) mRNAs in the nucleus, as well as increases the translation efficiency of ODC mRNA in the cytoplasm.
- CYBB is a common target gene repressed by HoxA10 and activated by HoxA9, and Meis1 and Nup98-hoxA9 have roles in repressing myeloid-specific gene transcription
- The HOXA9 protein expression was significantly downregulated in the MOF knockdown cells compared to control siRNA-treated cells.
- 90% of meningioma 1-ets variant gene 6 +/HOXA9+ mice developed AML much more rapidly than control HOXA9+ mice
- The relative HOXA9 expression was higher in patients in the accelerated phase of the disease (p<0.005). Interestingly, a patient with poorer prognosis (high Sokal's score), showing the highest HOXA9/ABL ratio, quickly entered a blast crisis and died.
- the expression of abd-b genes may be an imortant step involved in cervical cancer.
- The t(7;11)(p15;p15) translocation, observed in acute myelogenous leukemia and myelodysplastic syndrome, generates a chimeric gene where the 5' portion of the sequence encoding the human nucleoporin NUP98 protein is fused to the 3' region of HOXA9.
- Pim1 appears to be a direct transcriptional target of HOXA9 and a mediator of its antiapoptotic and proproliferative effects in early cells
- HOXA9 participates in the transcriptional activation of SELE in endothelial cells.
- HOXA9 inhibits endothelial cell activation downstream of NF-kappaB nuclear localization by interfering with NF-kappaB DNA binding, but not transactivation capacity
- DNA hypermethylation of tumour suppressor genes seems to play an important role in ovarian carcinogenesis and HOXA9, HOXB5, SCGB3A1, and CRABP1 are identified as novel hypermethylated target genes in this tumour type
- In this expt. mice with a compound deficiency in hoxa9, hoxb3 and hoxb4 (hoxa9/b3/b4) were investigated for evidence of synergy between these genes in hematopoiesis.
- In hypertensive patients, downregulation of HOXA9 expression in peripheral CD34+ cells may have a role in the loss of circulating endothelial progenitor cells, potentially impairing postnatal neovascularization and vascular repair.
- nuclear factor-kappaB (NF-kappaB) activation is an essential step for HOXA9 downregulation. And HOXA9 regulates its own expression by positive feedback mechanism.
- HoxA9 overexpression induces IGF-1R expression and subsequently promotes leukemic cell growth
- analysis of the role of deregulated PcG genes in acute myeloid leukemia, and the downstream PcG targets HOXA4, HOXA9 and MEIS1
- miR-126 may function in normal hematopoietic cells to modulate HOXA9 protein.
- HOXA9 overexpression is associated with acute myeloid leukemias.