c-Myc Antibody | Affinity Biosciences LTD|亲科生物官网

产品:	c-Myc 抗体
货号:	AF0358
描述:	Rabbit polyclonal antibody to c-Myc
应用:	WB IHC IF/ICC
反应:	Human, Mouse, Rat
预测:	Pig, Bovine, Horse, Sheep, Rabbit, Dog, Chicken, Xenopus
分子量:	49kDa; 49kD(Calculated).
蛋白号:	P01106
RRID:	AB_2833523

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二抗
封闭肽

阻断肽(封闭肽)是特异性结合目标抗体和阻断抗体结合的多肽。这些多肽包含抗体识别的抗原表位。与阻断肽结合的抗体不再与靶蛋白上的表位结合。例如，在免疫印迹(WB)和免疫组化(IHC)中，通过比较被阻断抗体和未阻断抗体的染色，可以看到哪种染色是特异性的。

规格	价格	库存
50ul	RMB¥ 1250	现货
100ul	RMB¥ 2300	现货
200ul	RMB¥ 3000	现货

货期: 当天发货

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实验方案

产品描述

来源:

Rabbit

应用:

WB 1:500-1:3000, 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(100%), Horse(100%), Sheep(100%), Rabbit(100%), Dog(100%), Chicken(100%), Xenopus(100%)

克隆:

Polyclonal

特异性:

c-Myc Antibody detects endogenous levels of total c-Myc.

RRID:

AB_2833523
引用格式: Affinity Biosciences Cat# AF0358, RRID:AB_2833523.

偶联:

Unconjugated.

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:

P01106(MYC_HUMAN) >>Visit HPA database.

基因/基因ID:

MYC(4609)

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:

P01106 MYC_HUMAN:
Protein BLAST With
NCBI/
ExPASy/
Uniprot

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

Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

翻译修饰 - P01106 作为底物

P01106

Site	PTM Type	Enzyme	Source
	Ubiquitination		Uniprot
S6	Phosphorylation		Uniprot
T8	Phosphorylation	P04049 (RAF1)	Uniprot
Y12	Phosphorylation		Uniprot
Y16	Phosphorylation		Uniprot
Y22	Phosphorylation		Uniprot
Y32	Phosphorylation	P00519 (ABL1)	Uniprot
K51	Sumoylation		Uniprot
K51	Ubiquitination		Uniprot
K52	Sumoylation		Uniprot
K52	Ubiquitination		Uniprot
T58	O-Glycosylation		Uniprot
T58	Phosphorylation	P49841 (GSK3B) , P28482 (MAPK1) , P49840 (GSK3A) , P53779 (MAPK10) , P45983 (MAPK8)	Uniprot
S62	Phosphorylation	Q13627 (DYRK1A) , P45984 (MAPK9) , Q00535 (CDK5) , P28482 (MAPK1) , P45983 (MAPK8) , Q92630 (DYRK2) , P53779 (MAPK10) , P42345 (MTOR)	Uniprot
S64	Phosphorylation		Uniprot
S67	Phosphorylation		Uniprot
S71	Phosphorylation	P28482 (MAPK1) , P45984 (MAPK9) , P53779 (MAPK10) , P45983 (MAPK8)	Uniprot
Y74	Phosphorylation	P00519 (ABL1)	Uniprot
T78	Phosphorylation		Uniprot
S81	Phosphorylation		Uniprot
K143	Acetylation		Uniprot
K148	Acetylation		Uniprot
K148	Sumoylation		Uniprot
K148	Ubiquitination		Uniprot
S151	Phosphorylation		Uniprot
K157	Acetylation		Uniprot
K157	Sumoylation		Uniprot
K157	Ubiquitination		Uniprot
S161	Phosphorylation		Uniprot
T244	Phosphorylation		Uniprot
S249	Phosphorylation	P68400 (CSNK2A1)	Uniprot
S250	Phosphorylation	P68400 (CSNK2A1)	Uniprot
S252	Phosphorylation	P68400 (CSNK2A1) , P48729 (CSNK1A1)	Uniprot
K275	Acetylation		Uniprot
S277	Phosphorylation		Uniprot
S279	Phosphorylation		Uniprot
S281	Phosphorylation		Uniprot
S288	Phosphorylation		Uniprot
K289	Ubiquitination		Uniprot
S293	Phosphorylation		Uniprot
K298	Ubiquitination		Uniprot
K317	Acetylation		Uniprot
K317	Sumoylation		Uniprot
K323	Acetylation		Uniprot
K323	Sumoylation		Uniprot
K323	Ubiquitination		Uniprot
K326	Sumoylation		Uniprot
K326	Ubiquitination		Uniprot
S329	Phosphorylation	P11309 (PIM1) , Q9P1W9 (PIM2)	Uniprot
S337	Phosphorylation		Uniprot
T343	Phosphorylation		Uniprot
S344	Phosphorylation		Uniprot
S347	Phosphorylation	P68400 (CSNK2A1)	Uniprot
S348	Phosphorylation	P68400 (CSNK2A1)	Uniprot
T350	Phosphorylation		Uniprot
K355	Sumoylation		Uniprot
K355	Ubiquitination		Uniprot
T358	Phosphorylation	Q13177 (PAK2)	Uniprot
K371	Acetylation		Uniprot
S373	Phosphorylation	Q13177 (PAK2)	Uniprot
K389	Sumoylation		Uniprot
K389	Ubiquitination		Uniprot
K392	Sumoylation		Uniprot
K392	Ubiquitination		Uniprot
K398	Sumoylation		Uniprot
K398	Ubiquitination		Uniprot
T400	Phosphorylation	Q13177 (PAK2)	Uniprot
S405	Phosphorylation		Uniprot
K412	Sumoylation		Uniprot
K412	Ubiquitination		Uniprot
K422	Ubiquitination		Uniprot
K430	Sumoylation		Uniprot
K430	Ubiquitination		Uniprot

研究背景

P01106_MYC_HUMAN

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.

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). Gut dysbiosis promotes prostate cancer progression and docetaxel resistance via activating NF-κB-IL6-STAT3 axis. Microbiome, 2022 (PubMed: 35710492) [IF=15.5]

Application: WB Species: Mouse Sample: tumor tissue

Fig. 4 The IL6-STAT3 pathway promoted prostate cancer proliferation. A Western blot of relative proteins in RM-1 and DU-145 cultured with CM or CM with Stattic for 24 h. B, C Edu (scale bar, 100 μm) and clone formation assay were conducted on RM-1 and DU-145 under condition as described. D Flowchart of the NC, Abx, and Abx+Stattic groups for in vivo study. Relevant tumor images and comparison of volume and weight for tumors in three groups (n = 5). E Immunohistochemistry of tumor tissues for p-STAT3-, c-myc-, and cyclin D1-positive cell in three groups (scale bar, 50 μm). Statistical significance was assessed by LSD in one-way ANOVA. *p < 0.05, **p < 0.01, and ***p < 0.001: compared to the NC group; #p < 0.05, ##p < 0.01, and ###p < 0.001: compared to the CM or Abx group

Application: IHC Species: Mouse Sample: tumor tissue

2). 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=14.9]

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).

3). Disordered farnesoid X receptor signaling is associated with liver carcinogenesis in Abcb11-deficient mice. The Journal of pathology, 2021 (PubMed: 34410012) [IF=7.3]

4). PIGU promotes hepatocellular carcinoma progression through activating NF-κB pathway and increasing immune escape. LIFE SCIENCES, 2020 (PubMed: 32971102) [IF=6.1]

Application: WB Species: Human Sample: HCC cells

Figure 2 PIGU knockdown inhibits proliferation and promotes apoptosis of HCC cells. After Hep-3B and Huh-7 cells were transfected with si-PIGU 1, si-PIGU 2, or its NC for 48 h, the mRNA and protein expression levels of PIGU were determined by RT-qPCR and Western blotting (A and B), cell viability was determined by CCK-8 assay (C and D), cell cycle distribution and apoptosis was evaluated by flow cytometry analysis (E and F), c-Myc, PCNA, cyclin D1, cleaved-caspase 3, and cleaved-PARP protein levels were detected by Western blotting (G). The densitometry of each band was normalized with that of respective β-actin. Data are means ± SD, n = 3. *P < 0.05 compared with si-NC group. PIGU, phosphodylinositol glycan anchor biosynthesis class U; RT-qPCR, quantitative Real-Time PCR; CCK-8, cell counting kit-8; SD, standard deviation; NC, negative control.

5). 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).

6). RECQL4 regulates DNA damage response and redox homeostasis in esophageal cancer. Cancer Biology & Medicine, 2021 (PubMed: 33628589) [IF=5.5]

Application: WB Species: Human Sample: KYSE30 and TE-1 cells

Figure 4 The loss of RECQL4 induces cell cycle arrest and cellular senescence. (A) Depletion of RECQL4 by siRNA. RECQL4 protein levels were measured by Western blot. KYSE30 and TE-1 cells were transfected with siRNA duplexes (200 nM) specific to RECQL4 or negative oligo in serum-free medium for 4 h, then replaced with complete medium for 24 h. Whole cell extracts were collected for Western blot analysis using RECQL4 antibodies. (B) Cell cycle distributions in RECQL4 knockdown cell lines (KYSE30 and TE-1 cells) and controls were determined by flow cytometry. (C) Cellular senescence was examined by SA-β-gal staining. Microscopic magnification (×200), Scale bar: 50 μm. (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.

7). 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]

Application: WB Species: mouse Sample: J774A. 1 cells

FIGURE 2|FKN promoted the viability of J774A.1 cells via Wnt/β-catenin signalling.D, E,Western blotting analysis and their respective quantitation showing the protein expression of FKN, β-catenin,Wnt-4, c-myc and cyclinD1 in J774A.1 cells.

Application: WB Species: Mice Sample: J774A.1 cells

FIGURE 2 FKN promoted the viability of J774A.1 cells via Wnt/β‐catenin signalling. A, B, Cells were incubated with Wnt3a (25, 50 and 75 ng/ml) and ICG‐001 (5, 10 and 15 μM/ml) for 24, 48 and 72 h. The viability of cells was estimated using the CCK‐8 assay. C, IF assay for KI67 in J774A.1 cells. D, E, Western blotting analysis and their respective quantitation showing the protein expression of FKN, β‐catenin, Wnt‐4, c‐myc and cyclinD1 in J774A.1 cells. F, The secretion of cyclinD1 in J774A.1 cell supernatants was detected using ELISA. * P < .05 compared with the control group; # P < .05 compared with the LPS group. G, The subcellular localization of cyclin D1 was identified by immunostaining using anti‐Cyclin D1 and observed using confocal microscopy. Scale bars represent 10 μm

8). 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=5.2]

9). Neuron specific enolase promotes tumor metastasis by activating the Wnt/β-catenin pathway in small cell lung cancer. Translational Oncology, 2021 (PubMed: 33618068) [IF=5.0]

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 

10). Neuron Specific Enolase Promotes Metastasis by Activating the Wnt/β-catenin Pathway in Small Cell Lung Cancer. Translational Oncology, 2020 (PubMed: 33618068) [IF=5.0]

Application: WB Species: human Sample: NSE-overexpressing H446 cells

Fig. 4. |Wnt/β-catenin signaling pathway was activated in NSE-overexpressing SCLC cells.(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.

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.

Application: WB Species: Human Sample: SCLC cells

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c-Myc Antibody - #AF0358

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