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Phospho-MAX (S2) Antibody

  • 中文名稱(chēng):
    磷酸化-MAX (S2)兔多克隆抗體
  • 貨號(hào):
    CSB-PA010069
  • 規(guī)格:
    ¥880
  • 其他:

產(chǎn)品詳情

  • Uniprot No.:
  • 基因名:
  • 別名:
    MAX antibody; BHLHD4Protein max antibody; Class D basic helix-loop-helix protein 4 antibody; bHLHd4 antibody; Myc-associated factor X antibody
  • 宿主:
    Rabbit
  • 反應(yīng)種屬:
    Human,Mouse,Rat
  • 免疫原:
    Synthesized peptide derived from Human Max around the phosphorylation site of S2.
  • 免疫原種屬:
    Homo sapiens (Human)
  • 標(biāo)記方式:
    Non-conjugated
  • 抗體亞型:
    IgG
  • 純化方式:
    The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
  • 濃度:
    It differs from different batches. Please contact us to confirm it.
  • 保存緩沖液:
    Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
  • 產(chǎn)品提供形式:
    Liquid
  • 應(yīng)用范圍:
    IHC, ELISA
  • 推薦稀釋比:
    Application Recommended Dilution
    IHC 1:100-1:300
    ELISA 1:5000
  • Protocols:
  • 儲(chǔ)存條件:
    Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
  • 貨期:
    Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.

產(chǎn)品評(píng)價(jià)

靶點(diǎn)詳情

  • 功能:
    Transcription regulator. Forms a sequence-specific DNA-binding protein complex with MYC or MAD which recognizes the core sequence 5'-CAC[GA]TG-3'. The MYC:MAX complex is a transcriptional activator, whereas the MAD:MAX complex is a repressor. May repress transcription via the recruitment of a chromatin remodeling complex containing H3 'Lys-9' histone methyltransferase activity. Represses MYC transcriptional activity from E-box elements.
  • 基因功能參考文獻(xiàn):
    1. MAX inactivation is a common event in GIST progression, fostering cell cycle activity in early GISTs. PMID: 28270683
    2. MAX to MYCN ratio that can account for tumour progression and clinical outcome in neuroblastoma. PMID: 29408445
    3. To our knowledge, this is the first report of an association between dysregulation of the MAX-MYC network in the brain and a behavior, suggesting a novel approach for exploiting the neuroplasticity associated with depression PMID: 27727240
    4. Sequence-specific DNA binding by MYC/MAX to low-affinity non-E-box motifs PMID: 28719624
    5. The SDHA, TMEM127, MAX, and SDHAF2 genes contribute to hereditary pheochromocytoma and paraganglioma. PMID: 28384794
    6. These results suggest that the wild type Max homodimer is important for attenuating the binding of c-Myc to specific and non-specific DNA, whereas alternative splicing (e.g. DeltaMax) is unable to do so. Conversely, the splicing of Max into DeltaMax could provoke an increase in overall chromatin bound c-Myc. PMID: 28350847
    7. evidence that MAX can 'sense' the oxidation status of 5mCpGs, and that cancer-associated mutations in MAX differentially affect binding to these features PMID: 27903915
    8. The mechanism of inhibition of c-Myc transcriptional activity by Miz-1 that binds c-Myc while competing for binding with Max has been described. PMID: 27859590
    9. The introduction of wild-type MAX cDNA into PC12 cells significantly decreased MYC's ability to bind to canonical E-boxes, while pathogenic MAX proteins were not able to fully repress MYC activity. Further clinical and molecular evaluation of variant carriers corroborated the results obtained with the functional assessment. PMID: 26070438
    10. Celastrol and some of its quinone methidecontaining analogs directly inhibit c-Myc-Max heterodimers in tumor cells. PMID: 26474287
    11. our results confirm that MAX is a tumor suppressor gene for renal oncocytomas PMID: 26670126
    12. In addition, loss of function mutation of the MAX gene was identified for the first time in GIST, and a broader role for MAX in GIST progression was suggested. mechanism for a subset of sporadic gastrointestinal stromal tumors PMID: 26555092
    13. We confirmed that these dimeric inhibitors directly bind to Myc blocking its interaction with Max and affect transcription of MYC dependent genes. PMID: 25875098
    14. MYC is part of a network of bHLHLZ proteins centered on the MYC heterodimeric partner MAX and its counterpart, the MAX-like protein MLX. PMID: 24857747
    15. Myc and its obligate heterodimeric partner, Max, are integral to the coordinated recruitment and post-translational modification of components of the core transcriptional machinery. PMID: 24657798
    16. Here we review the activities of MYC, MNT and other MAX interacting proteins in the setting of T and B cell activation and oncogenesis PMID: 24731854
    17. MAX mutations remain unusual events in Swedish patients with pheochromocytoma and paraganglioma tumours. PMID: 23743562
    18. Hypoxia reduces MAX expression in endothelial cells by unproductive splicing PMID: 25451222
    19. Genetic and molecular findings provide powerful evidence that MAX is a tumor-suppressor gene involved in SCLC development. PMID: 24362264
    20. Max mutation is associated with pheochromocytomas and paragangliomas. PMID: 24676840
    21. Delta Max, but not full-length Max, rescues Myc-dependent glycolytic gene expression upon induced EGFRvIII loss, and correlates with hnRNPA1 expression and downstream Myc-dependent gene transcription in patients. PMID: 23707073
    22. Data show that Sirt1, p53, and p38(MAPK) are involved in the detrimental phenotype of Max-null ESCs. Analyses revealed these proteins are involved at varying levels to one another in the hierarchy of the pathway leading to cell death in Max-null ESCs. PMID: 22696478
    23. germline mutations in MAX are responsible for 1.12% of hereditary and sporadic pheochromocytoma and paraganglioma in patients without evidence of other known mutations PMID: 22452945
    24. New structural determinants for c-Myc specific heterodimerization with Max and development of a novel homodimeric c-Myc b-HLH-LZ. PMID: 22733550
    25. Max b-HLH-LZ can transduce into cells and inhibit c-Myc transcriptional activities PMID: 22384171
    26. Genetic variants in MAX does not contribute to the development of Lynch syndrome. PMID: 22086303
    27. The E-box binding factors Max/Mnt, MITF, and USF1 act coordinately with FoxO to regulate expression of proapoptotic and cell cycle control genes by phosphatidylinositol 3-kinase/Akt/glycogen synthase kinase 3 signaling. PMID: 21873430
    28. The transcription factors Max and RXRalpha bind directly to the miR-193a promoter and inhibit miR-193a expression during transformation, thereby activating the PLAU and K-Ras oncogenes. PMID: 21670079
    29. MAX mutations are associated with hereditary pheochromocytoma. PMID: 21685915
    30. Enforced miR-22 expression presumably lowers Max levels available for Myc binding, which differentially influenced the transcription of downstream targets of the Myc-Max complex. PMID: 20214878
    31. downregulation of MYCN was reflected in a decreased MYCN/Max DNA-binding activity while the Mnt/Max binding did not change during differentiation PMID: 15258910
    32. High levels of Max and stress-induced NFkappaB activation may result in elevated expression of Fas ligand in human lung cancer cells and possibly contribute to Fas ligand-associated immune escape mechanisms. PMID: 15302589
    33. C6-cer inhibited the DNA-binding function of the c-Myc/Max oncogene PMID: 16201965
    34. Binding affinities & thermodynamics of dimerization of Max-Max homodimer & c-Myc-Max & Mad-Max heterodimers were determined.c-Myc & Max form most stable heterodimer.Polylysine had little effect, polyglutamic acid stabilized both heterodimers & homodimers. PMID: 16475822
    35. results uncover novel post-translational modifications of Max and suggest the potential regulation of specific Max complexes by p300 and reversible acetylation PMID: 17217336
    36. The switch from Mnt-Max to Myc-Max during bile duct ligation (cholestasis) and in hepatocytes treated with lithocholic acid is responsible for the induction in p53 and cyclin D1 expression and contributes to apoptosis. PMID: 19086036

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  • 相關(guān)疾病:
    Pheochromocytoma (PCC)
  • 亞細(xì)胞定位:
    Nucleus. Cell projection, dendrite.
  • 蛋白家族:
    MAX family
  • 組織特異性:
    High levels found in the brain, heart and lung while lower levels are seen in the liver, kidney and skeletal muscle.
  • 數(shù)據(jù)庫(kù)鏈接:

    HGNC: 6913

    OMIM: 154950

    KEGG: hsa:4149

    STRING: 9606.ENSP00000351490

    UniGene: Hs.285354