c-Myc Antibody - #AF0358

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Product: c-Myc Antibody
Catalog: AF0358
Description: Rabbit polyclonal antibody to c-Myc
Application: WB IHC IF/ICC
Reactivity: Human, Mouse, Rat
Prediction: Pig, Bovine, Horse, Sheep, Rabbit, Dog, Chicken, Xenopus
Mol.Wt.: 49kDa; 49kD(Calculated).
Uniprot: P01106
RRID: AB_2833523

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 100ul $280 In stock
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MSDS
Data Sheet
COA
Protocols
WB Handbook
IHC Protocol
IF/ICC Protocol

Product Info

Source:
Rabbit
Application:
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: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Mouse,Rat
Prediction:
Pig(100%), Bovine(100%), Horse(100%), Sheep(100%), Rabbit(100%), Dog(100%), Chicken(100%), Xenopus(100%)
Clonality:
Polyclonal
Specificity:
c-Myc Antibody detects endogenous levels of total c-Myc.
RRID:
AB_2833523
Cite Format: Affinity Biosciences Cat# AF0358, RRID:AB_2833523.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
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.
Alias:

Fold/Unfold

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);

Immunogens

Immunogen:
Uniprot:

P01106(MYC_HUMAN) >>Visit HPA database.

Gene(ID):
MYC(4609)
Description:
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.
Sequence:
MPLNVSFTNRNYDLDYDSVQPYFYCDEEENFYQQQQQSELQPPAPSEDIWKKFELLPTPPLSPSRRSGLCSPSYVAVTPFSLRGDNDGGGGSFSTADQLEMVTELLGGDMVNQSFICDPDDETFIKNIIIQDCMWSGFSAAAKLVSEKLASYQAARKDSGSPNPARGHSVCSTSSLYLQDLSAAASECIDPSVVFPYPLNDSSSPKSCASQDSSAFSPSSDSLLSSTESSPQGSPEPLVLHEETPPTTSSDSEEEQEDEEEIDVVSVEKRQAPGKRSESGSPSAGGHSKPPHSPLVLKRCHVSTHQHNYAAPPSTRKDYPAAKRVKLDSVRVLRQISNNRKCTSPRSSDTEENVKRRTHNVLERQRRNELKRSFFALRDQIPELENNEKAPKVVILKKATAYILSVQAEEQKLISEEDLLRKRREQLKHKLEQLRNSCA

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

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

PTMs - P01106 As Substrate

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

Research Backgrounds

Function:

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).

PTMs:

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).

Subcellular Location:

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
Subunit Structure:

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.

Research Fields

· 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)

References

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

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
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

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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