MAX Antibody

中文名稱：

MAX兔多克隆抗體
貨號：

CSB-PA013527LA01HU
規格：

￥440
圖片：
Immunohistochemistry of paraffin-embedded human heart tissue using CSB-PA013527LA01HU at dilution of 1:100

Immunohistochemistry of paraffin-embedded human colon cancer using CSB-PA013527LA01HU at dilution of 1:100

Immunofluorescent analysis of Hela cells using CSB-PA013527LA01HU at dilution of 1:100 and Alexa Fluor 488-congugated AffiniPure Goat Anti-Rabbit IgG(H+L)
其他：

產品詳情
產品評價
相關產品
靶點詳情

產品詳情

產品名稱：

Rabbit anti-Homo sapiens (Human) MAX Polyclonal antibody
Uniprot No.：

P61244
基因名：

MAX
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
反應種屬：

Human
免疫原：

Recombinant Human Protein max protein (1-58AA)
免疫原種屬：

Homo sapiens (Human)

標記方式：

Non-conjugated

本頁面中的產品，MAX Antibody (CSB-PA013527LA01HU)，的標記方式是Non-conjugated。對于MAX Antibody，我們還提供其他標記。見下表：

標記方式	貨號	產品名稱	應用
HRP	CSB-PA013527LB01HU	MAX Antibody, HRP conjugated	ELISA
FITC	CSB-PA013527LC01HU	MAX Antibody, FITC conjugated
Biotin	CSB-PA013527LD01HU	MAX Antibody, Biotin conjugated	ELISA

克隆類型：

Polyclonal
抗體亞型：

IgG
純化方式：

>95%, Protein G purified
濃度：

It differs from different batches. Please contact us to confirm it.
保存緩沖液：

Preservative: 0.03% Proclin 300
Constituents: 50% Glycerol, 0.01M PBS, PH 7.4
產品提供形式：

Liquid
應用范圍：

ELISA, IHC, IF

推薦稀釋比：

Application	Recommended Dilution
IHC	1:20-1:200
IF	1:50-1:200

Protocols：

ELISA Protocol
Immunohistochemistry (IHC) Protocol
Immunofluorescence (IF) Protocol
儲存條件：

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.
用途：

For Research Use Only. Not for use in diagnostic or therapeutic procedures.

產品評價

靶點詳情

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：
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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相關疾?。?/div>
Pheochromocytoma (PCC)
亞細胞定位：

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.
數據庫鏈接：

HGNC: 6913

OMIM: 154950

KEGG: hsa:4149

STRING: 9606.ENSP00000351490

UniGene: Hs.285354

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