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Human Monoclonal MAZ Primary Antibody für ChIP, EMSA - ABIN2668733
Ashfield, Patel, Bossone, Brown, Campbell, Marcu, Proudfoot: MAZ-dependent termination between closely spaced human complement genes. in The EMBO journal 1995
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Human Polyclonal MAZ Primary Antibody für IHC, WB - ABIN2780422
Ray, Shakya, Ray: Vascular endothelial growth factor expression in arthritic joint is regulated by SAF-1 transcription factor. in Journal of immunology (Baltimore, Md. : 1950) 2007
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Human Polyclonal MAZ Primary Antibody für IHC, IP - ABIN257716
Franz, Greschik, Willmann, Ozretić, Jilg, Wardelmann, Jung, Buettner, Schüle: The histone code reader SPIN1 controls RET signaling in liposarcoma. in Oncotarget 2015
Human Polyclonal MAZ Primary Antibody für WB - ABIN2778295
Himeda, Ranish, Hauschka: Quantitative proteomic identification of MAZ as a transcriptional regulator of muscle-specific genes in skeletal and cardiac myocytes. in Molecular and cellular biology 2008
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genotypes TT (SHMT1 rs4925166), CC (ERG rs2836425), GG (MAZ rs34286592), and GG (SHMT1 rs1979277) had the highest negative association (protective effect) with multiple sclerosis
MAZ is a potential therapeutic target to dampen STAT3 signaling in colon cancer.
High MAZ expression is associated with pancreatic cancer cell invasion.
MAZ can promote the invasion and metastasis of hepatocellular carcinoma by inducing epithelial-mesenchymal transition (EMT).
A quantitative association between MAZ-autoantibody optical density on ELISA and the cumulative inflammatory burden of atherosclerosis on (18)F-FDG PET/CT could be shown, suggesting MAZ-Ab as potential biomarker for atherosclerotic disease.
The data indicate that MAZ is essential to bypass MYB promoter repression by RB family members and to induce MYB expression.
MAZ/FOXF2 axis can promote the proliferation of basal like breast cancer cells and suppress disease progression.
Data suggest that long noncoding RNA PlncRNA1 and microRNA miR-34c bound together to regulate the expressions of MAZ, ZO-1 and occludin.
a transcriptional factor, Myc-associated zinc finger protein (MAZ), plays an important role in ADAM10 transcription in response to CT-1 in neural stem/progenitor cells.
Akt phosphorylates MAZ at Thr385, and the phosphorylated MAZ is released from the p53 promoter, leading to transcriptional activation of p53.
Myc-associated zinc-finger protein (MAZ) was identified as a direct target of miR-449a, mediating the tumor-suppressive effects.
Studies show a feed-forward regulatory pathway in breast cancer cells where SAF-1 acts as a transcriptional inducer of Ras which in turn increases DNA-binding and transcriptional activities of SAF-1 which in turn, increases transcription of Ras.
In conclusion, our present study indicated that miR-34c regulated the permeability of BTB via MAZ-mediated expression changes of ZO-1, occludin, and claudin-5.
Role of MAZ in prostate cancer and its interaction with androgen receptor were investigated. siRNA knockdown of AR significantly decreased MAZ expression, and knockdown of MAZ significantly increased the expression of AR.
these findings reveal that SAF-1 is a hitherto unrecognized participant in inducing VEGF expression in triple-negative breast cancer cells, an aggressive form of breast cancer that currently lacks effective treatment options.
relative abundance of SAF-2 plays a critical role in the fine tuned regulation of inflammation-responsive genes that are controlled by SAF-1
epitope spreading between the Tr antigen and the MAZ-DCC complex offers a possible model of immune-mediated cerebellar disease.
A novel promoter element was detected in the human MMP1 gene, and the inflammation-responsive transcription factor SAF-1 was found to interact with it in osteoarthritis
The putative -45 to -39 MYC-associated zinc finger protein-binding site regulates the constitutive activity of human PTHR1 P2 promoter.
SAF-1 controls cell cycle progression via p21 induction, and pathophysiological conditions that favor overexpression of SAF-1, such as an acute inflammatory condition, can trigger cellular growth arrest.
myc-associated zinc finger (MAZ) protein was essential for HIF2alpha activation of the Cav1 promoter.
HNF4-1 and MAZ-1 regulate the expression of Rho-GDIgamma and contribute to the differentiation of neural stem cells.
These data support a transcription mechanism for murine KRAS that involves MAZ, PARP-1 and duplex-quadruplex conformational changes in the promoter G-rich nuclease hypersensitive element.
SAF-1 induces VEGF transcription by directly binding to its promoter; markedly higher levels of SAF-1 interaction with the VEGF promoter was detected in the cartilage tissues of arthritic mice as well as human osteoarthritic patients.
These findings are consistent with a previously unrecognized role for MAZ in muscle gene regulation.
May function as a transcription factor with dual roles in transcription initiation and termination. Binds to two sites, ME1a1 and ME1a2, within the MYC promoter having greater affinity for the former. Also binds to multiple G/C-rich sites within the promoter of the Sp1 family of transcription factors.
, myc-associated zinc finger protein
, purine-binding transcription factor
, serum amyloid A activating factor 1
, serum amyloid A activating factor 2
, serum amyloid A-activating factor-1
, transcription factor Zif87
, zinc finger protein 801
, zinc-finger protein, 87 kilodaltons
, serum amyloid A-activating factor SAF-1