产品: c-Myc 抗体
货号: AF6054
描述: Rabbit polyclonal antibody to c-Myc
应用: WB IHC IF/ICC
文献验证: WB, IHC
反应: Human, Mouse, Rat
预测: Pig, Bovine, Horse, Sheep, Rabbit, Dog, Chicken, Xenopus
分子量: 50kDa; 49kD(Calculated).
蛋白号: P01106
RRID: AB_2834973

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产品描述

来源:
Rabbit
应用:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

反应:
Human, Mouse, Rat
预测:
Pig(100%), Bovine(%), Horse(%), Sheep(%), Rabbit(%), Dog(%), Chicken(%), Xenopus(%)
克隆:
Polyclonal
特异性:
c-Myc Antibody detects endogenous levels of total c-Myc.
RRID:
AB_2834973
引用格式: Affinity Biosciences Cat# AF6054, RRID:AB_2834973.
偶联:
Unconjugated. 130
纯化:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
保存:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
别名:

展开/折叠

AU016757; Avian myelocytomatosis viral oncogene homolog; bHLHe39; c Myc; Class E basic helix-loop-helix protein 39; MRTL; Myc; Myc protein; Myc proto oncogene protein; Myc proto-oncogene protein; myc-related translation/localization regulatory factor; MYC_HUMAN; Myc2; MYCC; Myelocytomatosis oncogene; Niard; Nird; Oncogene Myc; OTTHUMP00000158589; Proto-oncogene c-Myc; Protooncogene homologous to myelocytomatosis virus; RNCMYC; Transcription factor p64; Transcriptional regulator Myc-A; V-Myc avian myelocytomatosis viral oncogene homolog; v-myc myelocytomatosis viral oncogene homolog (avian);

抗原和靶标

免疫原:
Uniprot:
基因/基因ID:
描述:
Myc a proto-oncogenic transcription factor that plays a role in cell proliferation, apoptosis and in the development of human tumors.. Seems to activate the transcription of growth-related genes.
序列:
MPLNVSFTNRNYDLDYDSVQPYFYCDEEENFYQQQQQSELQPPAPSEDIWKKFELLPTPPLSPSRRSGLCSPSYVAVTPFSLRGDNDGGGGSFSTADQLEMVTELLGGDMVNQSFICDPDDETFIKNIIIQDCMWSGFSAAAKLVSEKLASYQAARKDSGSPNPARGHSVCSTSSLYLQDLSAAASECIDPSVVFPYPLNDSSSPKSCASQDSSAFSPSSDSLLSSTESSPQGSPEPLVLHEETPPTTSSDSEEEQEDEEEIDVVSVEKRQAPGKRSESGSPSAGGHSKPPHSPLVLKRCHVSTHQHNYAAPPSTRKDYPAAKRVKLDSVRVLRQISNNRKCTSPRSSDTEENVKRRTHNVLERQRRNELKRSFFALRDQIPELENNEKAPKVVILKKATAYILSVQAEEQKLISEEDLLRKRREQLKHKLEQLRNSCA

种属预测

种属预测:

score>80的预测可信度较高,可尝试用于WB检测。*预测模型主要基于免疫原序列比对,结果仅作参考,不作为质保凭据。

Species
Results
Score
Pig
100
Horse
100
Bovine
100
Sheep
100
Dog
100
Xenopus
100
Chicken
100
Rabbit
100
Zebrafish
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

研究背景

功能:

Transcription factor that binds DNA in a non-specific manner, yet also specifically recognizes the core sequence 5'-CAC[GA]TG-3'. Activates the transcription of growth-related genes. Binds to the VEGFA promoter, promoting VEGFA production and subsequent sprouting angiogenesis. Regulator of somatic reprogramming, controls self-renewal of embryonic stem cells. Functions with TAF6L to activate target gene expression through RNA polymerase II pause release (By similarity).

翻译修饰:

Phosphorylated by PRKDC. Phosphorylation at Ser-329 by PIM2 leads to the stabilization of MYC (By similarity). Phosphorylation at Ser-62 by CDK2 prevents Ras-induced senescence. Phosphorylated at Ser-62 by DYRK2; this primes the protein for subsequent phosphorylation by GSK3B at Thr-58. Phosphorylation at Thr-58 and Ser-62 by GSK3 is required for ubiquitination and degradation by the proteasome.

Ubiquitinated by the SCF(FBXW7) complex when phosphorylated at Thr-58 and Ser-62, leading to its degradation by the proteasome. In the nucleoplasm, ubiquitination is counteracted by USP28, which interacts with isoform 1 of FBXW7 (FBW7alpha), leading to its deubiquitination and preventing degradation. In the nucleolus, however, ubiquitination is not counteracted by USP28 but by USP36, due to the lack of interaction between isoform 3 of FBXW7 (FBW7gamma) and USP28, explaining the selective MYC degradation in the nucleolus. Also polyubiquitinated by the DCX(TRUSS) complex. Ubiquitinated by TRIM6 in a phosphorylation-independent manner (By similarity).

细胞定位:

Nucleus>Nucleoplasm. Nucleus>Nucleolus.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
亚基结构:

Efficient DNA binding requires dimerization with another bHLH protein. Binds DNA as a heterodimer with MAX. Interacts with TAF1C and SPAG9. Interacts with PARP10. Interacts with KDM5A and KDM5B. Interacts (when phosphorylated at Thr-58 and Ser-62) with FBXW7. Interacts with PIM2. Interacts with RIOX1. The heterodimer MYC:MAX interacts with ABI1; the interaction may enhance MYC:MAX transcriptional activity. Interacts with TRIM6 (By similarity). Interacts with NPM1; the binary complex is recruited to the promoter of MYC target genes and enhances their transcription. Interacts with CIP2A; leading to the stabilization of MYC.

研究领域

· Cellular Processes > Cell growth and death > Cell cycle.   (View pathway)

· Cellular Processes > Cell growth and death > Cellular senescence.   (View pathway)

· Cellular Processes > Cellular community - eukaryotes > Signaling pathways regulating pluripotency of stem cells.   (View pathway)

· Environmental Information Processing > Signal transduction > MAPK signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > ErbB signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > PI3K-Akt signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Wnt signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > TGF-beta signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Hippo signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Jak-STAT signaling pathway.   (View pathway)

· Human Diseases > Infectious diseases: Viral > Hepatitis B.

· Human Diseases > Infectious diseases: Viral > HTLV-I infection.

· Human Diseases > Infectious diseases: Viral > Epstein-Barr virus infection.

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

· Human Diseases > Cancers: Overview > Transcriptional misregulation in cancer.

· Human Diseases > Cancers: Overview > Proteoglycans in cancer.

· Human Diseases > Cancers: Overview > MicroRNAs in cancer.

· Human Diseases > Cancers: Specific types > Colorectal cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Endometrial cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Thyroid cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Bladder cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Chronic myeloid leukemia.   (View pathway)

· Human Diseases > Cancers: Specific types > Acute myeloid leukemia.   (View pathway)

· Human Diseases > Cancers: Specific types > Small cell lung cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Breast cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Hepatocellular carcinoma.   (View pathway)

· Human Diseases > Cancers: Specific types > Gastric cancer.   (View pathway)

· Human Diseases > Cancers: Overview > Central carbon metabolism in cancer.   (View pathway)

· Organismal Systems > Endocrine system > Thyroid hormone signaling pathway.   (View pathway)

文献引用

1). Upregulation of BCL-2 by acridone derivative through gene promoter i-motif for alleviating liver damage of NAFLD/NASH. NUCLEIC ACIDS RESEARCH, 2020 (PubMed: 32710621) [IF=16.6]

Application: WB    Species: human    Sample: HepG2

Figure 3. Effect of A22 on gene transcription and translation in HepG2 cells. The mRNA levels of BCL-2 and BAX (A), as well as C-KIT, KRAS, C-MYC and VEGF (B) in HepG2 cells were analyzed by using qRT-PCR after incubation with increasing concentration of A22 for 12 h. (C) Effects of A22 on protein expressions of C-MYC, VEGF, C-KIT and BCL-2 in the presence or absence of increasing concentration of A22 for 24 h, which were quantitatively analyzed (D).

2). Target deubiquitinase OTUB1 as a therapeatic strategy for BLCA via β-catenin/necroptosis signal pathway. International journal of biological sciences, 2024 (PubMed: 39113709) [IF=8.2]

Application: WB    Species: Mouse    Sample: BLCA cells

Figure 7. OTUB1 is involved in cisplatin resistance of BLCA through β-catenin stabilization. A. Cell survival assay was determined in T24 control cell and T24 cisplatin-resistance cell. B. The changes in cell morphology between the T24 control cell and the T24 cisplatin-resistance cell. C. Relative expression of several chemoresistance markers (including MDR1, BCRP and YB-1) in T24 control cell and T24 cisplatin-resistance cell with or without cisplatin treatment. D. Relative expression of OTUB1 in T24 control cell and T24 cisplatin-resistance cell with or without cisplatin treatment. E. Relative expression of OTUB1, necroptosis-related markers (such as RIPK3, MLKL and P-MLKL), β-catenin and downstream proteins (including AXIN-2, C-myc, cyclin D1 and TCF1) in T24 cisplatin-resistance cells treated with gradient cisplatin concentration. F. Immunoprecipitation assay showed the relationship between OTUB1 and β-catenin in T24 cisplatin-resistance cells. G. Immunoprecipitation assay showed that gradient cisplatin concentration promotes the interaction between OTUB1 and β-catenin, and restrains the ubiquitination of β-catenin. H. Relative expression of OTUB1, necroptosis-related markers (such as RIPK3, MLKL and P-MLKL), β-catenin and downstream targets following elevated OTUB1, β-catenin with or without XAV-939 treatment in T24 cisplatin-resistance cell (control, OTUB1, OTUB1/XAV-939, β-catenin). I. Cell survival assay was determined in T24 cisplatin-resistance cells following overexpressed OTUB1 with or without 10uM XAV-939 (or knockdown OTUB1 with or without overexpressed β-catenin). J. Knockdown OTUB1 restrains the growth in T24 cisplatin-resistance mice bladder tumor in vivo.

3). Exosome-derived long non-coding RNA AC010789.1 modified by FTO and hnRNPA2B1 accelerates growth of hair follicle stem cells against androgen alopecia by activating S100A8/Wnt/β-catenin signalling. Clinical and translational medicine, 2025 (PubMed: 39748192) [IF=7.9]

Application: WB    Species: Mouse    Sample: HFSCs

FIGURE 5 S100A8 was identified as a downstream regulator of AC010789.1 to promote hair follicle stem cells (HFSCs) growth by activating Wnt/β-catenin signalling (A) RNA pull-down analysis of the interaction of S100A8 protein with the AC010789.1 mRNAs in HFSCs. (B) RIP analysis of the endogenous enrichment of AC010789.1 mRNAs in S100A8 protein in HFSCs. (C, D) Real-time quantitative polymerase chain reaction (qRT-PCR) and Western blot analysis of the expression levels of S100A8 after the transfection with AC010789.1 OE lentiviruses or si-AC010789.1 into HFSCs. (E, F) qRT-PCR and Western blot analysis of the expression levels of S100A8, K6HF and Lgr5 after the transfection of si-AC010789.1 into HFSCs. (G-I) CCK8, 5-ethynyl-2'-deoxyuridine assay (EdU) and Transwell analysis of the cell proliferation and migration viability after the co-transfection with AC010789.1 OE lentiviruses and si-S100A8 into HFSCs. (J) Western blot analysis of the expression levels of S100A8, Wnt10b, β-catenin and c-myc after the co-transfection with AC010789.1 OE lentiviruses and si-S100A8 into HFSCs. Data shown are the mean ± SEM of three experiments. **p < .01, ***p < .001 and ****p < .0001.

4). Silencing c-Myc Enhances the Antitumor Activity of Bufalin by Suppressing the HIF-1α/SDF-1/CXCR4 Pathway in Pancreatic Cancer Cells. Frontiers in Pharmacology, 2020 (PubMed: 32362830) [IF=5.6]

Application: WB    Species: Human    Sample: pancreatic cancer cells

Figure 1 Construction of the cell lines with different c-Myc expression. The expression of c-Myc in human pancreatic cancer cells (Colo357, HS766T, PANC-1, BxPC3, SW1990, PIC-35) was detected via (A) Quantitative real-time polymerase chain reaction (qRT-PCR) and (B) western blot (n = 3). The expression of c-Myc in PANC-1 cells transfected with si-c-Myc or siRNA negative control was detected via (C) qRT-PCR and (D) western blot (** p < 0.01 vs control, n = 3). The expression of c-Myc in SW1990 cells transfected with pcDNA-c-Myc or empty vector pcDNA was detected via (E) qRT-PCR and (F) western blot (** p < 0.01 vs control, n = 3).

5). RECQL4 regulates DNA damage response and redox homeostasis in esophageal cancer. Cancer Biology & Medicine, 2021 (PubMed: 33628589) [IF=5.6]

Application: WB    Species: human    Sample: ESCC cells

Figure 4 |The loss of RECQL4 induces cell cycle arrest and cellular senescence. . (D) The protein levels of c-myc, p21, cyclin D, CDK6, cyclin E, Bax, and Bcl-2 were determined by Western blot in stable Tet-on inducible RECQL4 knockdown cell lines (KYSE30 and TE-1 cells) (+Dox) and controls (–Dox). Experiments were independently repeated 3 times. All data indicate the mean ±SD. *P < 0.05; **P < 0.01; ***P < 0.001.

6). Fractalkine Aggravates LPS-induced Macrophage Activation and Acute Kidney Injury via Wnt/β-catenin Signaling Pathway. JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, 2021 (PubMed: 34101346) [IF=5.3]

7). PIGU promotes hepatocellular carcinoma progression through activating NF-κB pathway and increasing immune escape. LIFE SCIENCES, 2020 (PubMed: 32971102) [IF=5.2]

Application: IHC    Species: Human    Sample: HCC cells

Figure 7 PIGU knockdown suppresses tumorigenesis of HCC cells in vivo. (A) Relative protein expression levels of PIGU, c-Myc, MMP2, and cleaved-caspase 3 in tumor tissues measured by Western blotting. The densitometry of each band was normalized with that of respective β-actin. (B) The expression of PIGU, c-Myc, MMP2, and cleaved-caspase 3 in tumor tissues detected by immunohistochemistry staining. Scale bar = 50 μm. Data are means ± SD, n = 6. *P < 0.05 compared with shRNA-NC group. PIGU, phosphodylinositol glycan anchor biosynthesis class U; MMP2, matrix metalloproteinase 2; SD, standard deviation; NC, negative control.

8). Phillygenin Inhibits TGF-β1-induced Hepatic Stellate Cell Activation and Inflammation: Regulation of the Bax/Bcl-2 and Wnt/β-catenin Pathways. Inflammation, 2024 (PubMed: 38393550) [IF=4.5]

Application: WB    Species: Mouse    Sample: mHSC

Fig. 10 Efects of PHI on Wnt/β-catenin signaling pathway-related proteins. a Western blotting analyses of Wnt1, β-catenin, GSK-3β, p-GSK-3β, c-Myc, and Cyclin D1 in mHSCs.

9). Upregulation of E‑cadherin expression mediated by a novel dsRNA suppresses the growth and metastasis of bladder cancer cells by inhibiting β-catenin/TCF target genes. INTERNATIONAL JOURNAL OF ONCOLOGY, 2018 (PubMed: 29620261) [IF=4.5]

10). Neuron Specific Enolase Promotes Metastasis by Activating the Wnt/β-catenin Pathway in Small Cell Lung Cancer. Translational Oncology, 2020 (PubMed: 33618068) [IF=4.5]

Application: WB    Species: Human    Sample: SCLC cells

Fig. 4 Wnt/β-catenin signaling pathway was activated in NSE-overexpressing SCLC cells. (A) Signal pathway enrichment investigation between high NSE expression group and low NSE expression group was enriched by GSEA. (B, C) NSE overexpression activated Wnt/β-catenin pathway and upregulated the expression of downstream target genes (c-Myc and Slug). The protein (B) and mRNA (C) expression of β-catenin, c-Myc and Slug in NSE-overexpressing H446 cells were tested by western blotting and qRT-PCR, respectively. (D, E) Silencing NSE repressed Wnt/β-catenin signaling pathway. The protein (D) and mRNA (E) expression of β-catenin, c-Myc and Slug in NSE-silencing H69 cells. Results was representative of three independent experiments. Data are presented as mean values ± SD. *p < 0.05 using the two-sided Student's t-test. ns: no significance.

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