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anti-Human MYB Antibodies:
anti-Mouse (Murine) MYB Antibodies:
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Human Polyclonal MYB Primary Antibody for IHC (p), ELISA - ABIN545264
Luchetti, Paroncini, Majlingovà, Frampton, Mucenski, Baroni, Sambo, Golay, Introna, Gabrielli: Characterization of the c-Myb-responsive region and regulation of the human type I collagen alpha 2 chain gene by c-Myb. in The Journal of biological chemistry 2003
Show all 3 Pubmed References
Horse (Equine) Polyclonal MYB Primary Antibody for ELISA, WB - ABIN538321
Bies, Markus, Wolff: Covalent attachment of the SUMO-1 protein to the negative regulatory domain of the c-Myb transcription factor modifies its stability and transactivation capacity. in The Journal of biological chemistry 2002
Show all 2 Pubmed References
Human Polyclonal MYB Primary Antibody for IHC, WB - ABIN6713460
Bhattarai, Lee, Lee, Yi: Gene delivery of c-myb increases bone formation surrounding oral implants. in Journal of dental research 2013
Human Polyclonal MYB Primary Antibody for ELISA, ICC - ABIN6263448
Huang, Zhang, Hou, Wang, Liu, Zhang, Chen, Zhu: LncRNA AK023391 promotes tumorigenesis and invasion of gastric cancer through activation of the PI3K/Akt signaling pathway. in Journal of experimental & clinical cancer research : CR 2018
Dog (Canine) Polyclonal MYB Primary Antibody for ELISA, WB - ABIN547949
Clappier, Cuccuini, Kalota, Crinquette, Cayuela, Dik, Langerak, Montpellier, Nadel, Walrafen, Delattre, Aurias, Leblanc, Dombret, Gewirtz, Baruchel, Sigaux, Soulier: The C-MYB locus is involved in chromosomal translocation and genomic duplications in human T-cell acute leukemia (T-ALL), the translocation defining a new T-ALL subtype in very young children. in Blood 2007
Cow (Bovine) Polyclonal MYB Primary Antibody for ELISA, WB - ABIN4285666
Fahl, Crittenden, Allman, Bender: c-Myb is required for pro-B cell differentiation. in Journal of immunology (Baltimore, Md. : 1950) 2009
Study find that c-Myb is abnormally overexpressed in colorectal cancer (CRC) tissues and correlated with lymph node metastasis. High expression of c-Myb is an independent unfavorable factor affecting patient prognosis. c-Myb promotes the growth and metastasis of CRC cells through epithelial-mesenchymal transition by upregulating c-fos. These findings indicate that c-Myb is a promising prognostic indicator for CRC.
MiR-363-3p was significantly highly expressed in osteoporotic samples. Mechanistically, miR-363-3p promotes osteoclastogenesis and inhibits osteogenic differentiation by targeting PTEN and therefore activating PI3K/AKT signaling pathway. MiR-363-3p was activated by its upstream transcription activator MYB
We demonstrated that exosomes delivered miR-130a from gastric cancer cells into vascular cells to promote angiogenesis and tumor growth by targeting c-MYB both in vivo and in vitro. miR-130a packaged in exosomes secreted from cancer cells acts as a driver of angiogenesis.
Results demonstrated that MYB is aberrantly overexpressed in salivary adenoid cystic carcinoma (SACC) tissues, and promotes SACC cell proliferation and metastasis.
Breast adenoid cystic carcinomas probably constitute a convergent phenotype, whereby activation of MYB and MYBL1 and their downstream targets can be driven by the MYB-NFIB fusion gene, MYBL1 rearrangements, MYB amplification, or other yet to be identified mechanisms.
Data observe that increasing and decreasing the helical stability of c-Myb over a broad range has a small effect on the binding affinity to KIX domain of CREB binding protein. To reduce the binding affinity by more than 1 kcal/mol, it was necessary to introduce glycine or proline in the middle of the c-Myb helix.
In the present study, MYB or MYBL1 locus rearrangement was detected in nearly all adenoid cystic carcinoma cases, and therefore it would be a good diagnostic marker for adenoid cystic carcinoma.
Collectively, our data showed that ZFAS1 contributed to the development of AML by sequestering miR-150 from Myb or Sp1, elucidating the central roles of ZFAS1/miR-150/Myb and ZFAS1/miR-150/Sp1 pathways in the tumorigenesis of AML and deepening our understanding on the etiology of leukemia.
The presence of the MYB fusion in intermediate-grade and hybrid carcinomas that at least partially exhibit an epithelial-myoepithelial carcinoma phenotype may in fact point to an adenoid cystic carcinoma.
The c-Myb gene encodes a transcription factor that regulates cell proliferation, differentiation, and apoptosis through protein-protein interaction and transcriptional regulation of signaling pathways. The protein is frequently overexpressed in human leukemias, breast cancers, and solid tumors suggesting that it is a bona fide oncogene. c-MYB is often overexpressed by chromosomal translocation in human tumors. [review]
Low c-myb expression promotes breast cancer lung metastasis.
High c-myb expression is associated with In-Stent Restenosis in Peripheral Artery Disease.
Data provide evidences supporting the role of Sema5A in melanoma progression and the involvement of Bcl-2, miR-204 and c-Myb in regulating its expression.
The data demonstrate that c-Myb plays a critical role in the activation of NK cells and therefore is a therapeutic target for cancer and viral diseases.
found no significant differences in the genetic distribution and allelic frequency of MYB and SOX-6 gene polymorphisms
Salivary gland ACC cases expressing the MYB-NFIB chimeric gene showed significantly higher blood vessels density compared to non-expressing cases, and suggested that higher VEGF production capability in the former cases may be the cause. The findings also suggested that MYB-NFIB chimeric gene expression may be related to the onset age of ACC.
These results indicated that low expression of Mda-7/IL-24 along with high expression of C-myb are predictors for poor prognosis of Burkitt lymphoma patients; this outcome suggests that Mda-7/IL-24 and C-myb might be potential targets for clinical treatment of Burkitt lymphoma.
C-Myb expression in the laryngeal squamous cell carcinoma.YB-1 regulates miR-155 expression via c-Myb in the laryngeal squamous cell carcinoma.
Data indicate a pioneer factor model in which c-Myb binds to regions of closed chromatin and then recruits histone acetyltransferases. By binding to histones, c-Myb facilitates histone acetylation, acting as a cofactor for p300 at c-Myb binding sites. The resulting H3K27ac leads to chromatin opening and detachment of c-Myb from the acetylated chromatin.
Both cases harbored the MYB-NFIB gene fusion as demonstrated by FISH and RNA-sequencing
Findings identify myb proto-oncogene protein (c-Myb) as a pivotal regulator of CD8(+) T cell stemness and suggest its therapeutic potential.
This study provides evidence that c-Myb might serve as a new target for the prevention of aminoglycoside-induced hair cells loss.
these results identify a key role for miR-150 in memory CD8 T cells through a c-Myb-controlled enhanced survival circuit.
Myb knockdown in Setbp1 and Setbp1 missense mutations-induced AML cells also efficiently induced their differentiation in culture and significantly prolonged the survival of their secondary recipient mice.
These findings reveal miR-301b as a new controller of inflammatory response by repressing c-Myb function to inhibit the anti-inflammatory response to bacterial infection, representing a novel mechanism for balancing inflammation.
The analysis points to a critical role for Hoxa9 and PU.1 in distal regulation of c-myb expression in murine myeloid cells during iL-6-induced cell differentiation.
Data suggest that the upregulations of Myb and Peg3 are likely the key anti-cancer events of EGCG in vivo.
deficiency alters the expression of a crucial subset of TAL1- and NOTCH1-regulated genes, including the MYB and MYC oncogenes, respectively.
MYB acts on MAPK signaling by directly regulating transcription of the gene encoding the negative modulator SPRY2.
This work provides important mechanistic insight into how spatiotemporal expression of the Rag genes is tightly controlled during B lymphocyte development to prevent mistimed dsDNA breaks and their deleterious consequences.
These results Myb as a critical component of the gene regulatory network controlling effector Treg cell differentiation and function.
Production of dendritic-like cells and resident monocytes was not affected by the c-MybE308G mutation.
Myb expands the ISC pool within which CRC is initiated while co-operating with TSG loss
c-Myb regulates proliferation/differentiation of adventitial Sca1+ vascular smooth muscle progenitor cells by transcriptional activation of myocardin.
the key role of the transcription factor c-Myb in regulating the T-bet-mediated anti-viral program, is reported.
p38 and NOX1 are essential for the protective effect of c-Myb and that NOX1 acts upstream of p38 activation.
These findings reveal that miR-150 acts as a pivotal regulator of pressure overload-induced cardiac fibrosis by regulating c-Myb.
MYB and C/EBPalpha activities are inter-dependent in controlling Flt3 expression to influence lineage commitment of multipotential progenitors.
Myb regulates Cyclin E1 expression in normal gastrointestinal tract epithelial cells and is required during intestinal tumorigenesis
Zebrafish blastomere screen identifies retinoic acid suppression of MYB in adenoid cystic carcinoma.
studies show that merestinib effectively blocks eIF4E phosphorylation in AML cells and suppresses primitive leukemic progenitors from AML patients in vitro and in an AML xenograft model in vivo.
cMyb plays a hitherto unidentified role in dictating physiologic HSPC migration by modulating Sdf1a signaling.
show that knockdown of miR-126 results in increased c-Myb levels and promotes erythropoiesis at the expense of thrombopoiesis in vivo
Results suggest that the key role of c-myb in definitive hematopoiesis is similar to that in mammals and must have become established early in vertebrate evolution.
expression of CD41 and cmyb marks nascent HSCs in the zebrafish AGM, and provide the means to further dissect HSC generation and
This gene encodes a transcription factor that is a member of the MYB family of transcription factor genes. The protein contains three domains, an N-terminal DNA-binding domain, a central transcriptional activation domain and a C-terminal domain involved in transcriptional repression. This protein plays an essential role in the regulation of hematopoiesis and may play a role in tumorigenesis. Alternative splicing results in multiple transcript variants.
c-myb protein (140 AA)
, proto-oncogene c-Myb
, transcriptional activator Myb
, gag-myb protein
, myb proto-oncogene protein
, myeloblastosis proto-oncogene product
, tumor-specific myb protein
, myeloblastosis oncogene
, Avian myeloblastosis viral (v-myb) oncogene homolog
, v-myb myeloblastosis viral oncogene homolog (avian)
, transcriptional activator Myb-like
, DNA-binding transcriptional regulator
, c-myb proto-oncogene
, transcription factor cmyb
, v-myb myeloblastosis viral oncogene homolog
, v-myb avian myeloblastosis viral oncogene homolog