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Validated All-in-One™ qPCR Primer for MYB(NM_001130173.2) Search again
Product ID:
HQP130575
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
Cmyb, c-myb, c-myb_CDS, efg
Gene Description:
MYB proto-oncogene, transcription factor
Target Gene Accession:
NM_001130173.2(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.
Gene References into function
- Activation of c-MYC and c-MYB proto-oncogenes is associated with decreased apoptosis in tumor colon progression.
- Friend murine erythroleukemia cells are held in an immature and proliferating state by a pathway that is dependent on Myb activity
- c-Myb transactivates the IGFBP-5 promoter
- c-Myb has no apparent effect on core binding factor/polyoma enhancer-binding protein 2 binding, but is critical for activation of enhancer-dependent transcription of the TCR delta enhancer.
- role in regulating type I collagen alpha 2 chain gene
- involvement of c-myb in the regulation of intestinal nutrient absorption
- Data suggest that the negative influence on transactivation properties by the negative regulatory domain region of c-Myb depends on sumoylation sites.
- NmU expression is related to Myb and that the NmU/NMU1R axis constitutes a previously unknown growth-promoting autocrine loop in myeloid leukemia cells
- p53 antagonizes c-Myb by recruiting mSin3A to down-regulate specific Myb target genes
- c-Myb activity is directly regulated by cyclin D1 and CDKs and imply that c-Myb activity is regulated during the cell cycle in hematopoietic cells
- 10 genes were down-regulated following treatment of the T-ALL cells with 0.15 and 1.5 microg/mL of metal ores at 72 h.
- data suggest that amplification of c-myb in tumor cells may lead to robust GRP78 gene induction, which may in turn assist cells in survival under conditions of oxygen deprivation and nutrient stress
- c-Myb has a longer half-life (at least 2-fold) in BCR/ABL-expressing than in normal hematopoietic cells
- EGF-induced activation of B-Myb promoter required both E2F and EGFR target sites
- point mutation are uncommon in patients with myeloproliferative disorders
- c-Myb is a major factor that controls differentiation as well as proliferation of hematopoietic progenitor cells derived from hemogenic endothelial cells; appropriate levels of c-Myb protein are strictly defined at distinct differentiation steps
- Together, these results show that the cAMP pathway blocks gamma-globin gene expression in K562 cells by increasing c-Myb expression.
- The enhanced stability of c-Myb in CML blast crisis cells and perhaps in other types of leukemia is not caused by a genetic mechanism.
- individuals with elevated HbF levels during adult erythropoiesis demonstrated simultaneous transcriptional down-regulation in cMYB and HBS1L
- Among MYB regulation, the most dynamic is the control of transcriptional elongation by sequences within intron 1, this regulatory sequence is transcribed into an RNA stem-loop and 19-residue polyuridine tract, and is subject to mutation in colon cancer.
- a lack of integrin engagement leads to the induction of cellular markers associated with myeloid differentiation
- c-Myb protein plays a previously unappreciated role in the G(2)/M cell cycle transition of normal and malignant human hematopoietic cells
- c-Myb regulates cell cycle-associated IP3R1 transcription in VSMCs via specific highly conserved Myb-binding sites in the IP3R1 promoter.
- Duplication of MYB is an oncogenic event and we suggest that MYB could be a therapeutic target in human T cell acute lymphoblastic leukemia.
- The MYB(dup) alteration was associated with T-cell acute leukemia
- These experimental results suggested that ApoH may be one of the members of the regulator of circadian rhythm and that ApoH expression level was also dependent on circadian rhythm in Jurkat cells and in human plasma.
- CK2 phosphorylation triggers an allosteric inhibition of the SNAP190 Myb DNA binding domain
- MYB is an effector of estrogen/estrogen signaling
- The HBS1L-MYB intergenic region on chromosome 6q23.3 influences erythrocyte, platelet, and monocyte counts.
- Alu--mediated MYB tandem duplication occurs at low frequency during normal thymocyte development and is clonally selected during the molecular pathogenesis of human T-ALL
- TRAF6 is modified by small ubiquitin-related modifier-1, interacts with histone deacetylase 1, and represses c-Myb-mediated transactivation.
- An array of variant transcripts, expressed in highly regulated, lineage-specific patterns were formed from alternate exons 8A, 9A, 9B, 10A, 13A, & 14A. They encoded c-Myb proteins with identical DNA binding domains but unique C-terminal domains.
- c-Myb cooperates with FLASH in foci associated with active RNA polymerase II, leading to enhancement of Myb-dependent gene activation.
- MYB is highly expressed in almost all estrogen-receptor-positive breast tumours & is a direct target of estrogen/ER signalling. It is required for tumor cell proliferation. Review.
- These data provide evidence that c-Myb may serve a previously unappreciated role in the coupling between transcription and splicing.
- c-Myb is an evolutionally conserved target of miR-150 and miR-150/c-Myb interaction is important for embryonic development and possibly oncogenesis
- Fbxw7, the F-box protein of an SCF complex, targets c-Myb for degradation in a Wnt-1- and NLK-dependent manner.
- these findings suggest the presence of a c-Myb-miR-15a autoregulatory feedback loop of potential importance in human hematopoiesis
- a gain of the MYB locus, was found recurrently and only in the MYST3-linked AMLs (7/18 vs 0/34). MYST3-AMLs have also a specific a gene expression profile, which includes overexpression of MYB, CD4 and HOXA genes