Recombinant Human Transcription factor AP-1(JUN)

Code CSB-YP011972HU
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Source Yeast
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Code CSB-EP011972HU
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Source E.coli
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Code CSB-EP011972HU-B
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Source E.coli
Conjugate Avi-tag Biotinylated
E. coli biotin ligase (BirA) is highly specific in covalently attaching biotin to the 15 amino acid AviTag peptide. This recombinant protein was biotinylated in vivo by AviTag-BirA technology, which method is BriA catalyzes amide linkage between the biotin and the specific lysine of the AviTag.
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Code CSB-BP011972HU
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Source Baculovirus
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Code CSB-MP011972HU
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Source Mammalian cell
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Product Details

Purity >85% (SDS-PAGE)
Target Names JUN
Uniprot No. P05412
Alternative Names Activator protein 1; AP 1; AP-1; AP1; cJun; Enhancer Binding Protein AP1; Jun Activation Domain Binding Protein; JUN; Jun oncogene; JUN protein; Jun proto oncogene; JUN_HUMAN; JUNC; Oncogene JUN; p39; Proto oncogene c jun; Proto oncogene cJun; Proto-oncogene c-jun; Transcription Factor AP 1; Transcription factor AP-1; Transcription Factor AP1; V jun avian sarcoma virus 17 oncogene homolog; V jun sarcoma virus 17 oncogene homolog (avian); V jun sarcoma virus 17 oncogene homolog; V-jun avian sarcoma virus 17 oncogene homolog; vJun Avian Sarcoma Virus 17 Oncogene Homolog
Species Homo sapiens (Human)
Expression Region 1-331
Target Protein Sequence MTAKMETTFY DDALNASFLP SESGPYGYSN PKILKQSMTL NLADPVGSLK PHLRAKNSDL LTSPDVGLLK LASPELERLI IQSSNGHITT TPTPTQFLCP KNVTDEQEGF AEGFVRALAE LHSQNTLPSV TSAAQPVNGA GMVAPAVASV AGGSGSGGFS ASLHSEPPVY ANLSNFNPGA LSSGGGAPSY GAAGLAFPAQ PQQQQQPPHH LPQQMPVQHP RLQALKEEPQ TVPEMPGETP PLSPIDMESQ ERIKAERKRM RNRIAASKCR KRKLERIARL EEKVKTLKAQ NSELASTANM LREQVAQLKQ KVMNHVNSGC QLMLTQQLQT F
Protein Length Full length protein
Tag Info The following tags are available.
N-terminal His-tagged
Tag-Free
The tag type will be determined during production process. If you have specified tag type, please tell us and we will develop the specified tag preferentially.
Form Lyophilized powder
Buffer before Lyophilization Tris/PBS-based buffer, 6% Trehalose, pH 8.0
Reconstitution We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20℃/-80℃. Our default final concentration of glycerol is 50%. Customers could use it as reference.
Troubleshooting
and FAQs
Protein FAQs
Storage Condition Store at -20°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.
Notes Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet Please contact us to get it.

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Target Data

Function Transcription factor that recognizes and binds to the enhancer heptamer motif 5'-TGA[CG]TCA-3'. Promotes activity of NR5A1 when phosphorylated by HIPK3 leading to increased steroidogenic gene expression upon cAMP signaling pathway stimulation. Involved in activated KRAS-mediated transcriptional activation of USP28 in colorectal cancer (CRC) cells
Gene References into Functions
  1. data indicated that miR-139-5p was down-regulated in the hearts of Hypertrophic cardiomyopathy patients and that it inhibited cardiac hypertrophy by targetting c-Jun expression. PMID: 29440459
  2. this study identified an essential Jun/miR-22/HuR regulatory axis in CRC (the working model is summarised in Fig. 8) and highlighted the vital role of HuR and miR-22 in CRC proliferation and migration. PMID: 29351796
  3. a novel cascade mediated by AP-1 and FOXF1 that regulates oncogene-induced senescence, is reported. PMID: 30119690
  4. Multivalent Interactions with Fbw7 and Pin1 Facilitate Recognition of c-Jun by the Fbw7. PMID: 29225075
  5. High AP-1 expression is associated with metastasis in colon cancer. PMID: 29305742
  6. Our results suggest that extended AP-1 binding sites, together with adjacent binding sites for additional TFs, encode part of the information that governs transcription factor binding sites activity in the genome. PMID: 29305491
  7. the expression of WIF-1 was low in GBC cells due to aberrant hypermethylation of its promoter region. Additionally, an alternative pathogenesis of GBC was indicated in which c-Jun causes hypermethylation of the WIF-1 promoter region, and represses the expression of WIF-1 through transcriptional regulation and interaction with DNMT1 as an early event in the tumorigenesis of GBC. PMID: 29693707
  8. Mutant cellular AP-1 proteins promote expression of a subset of Epstein-Barr virus late genes in the absence of lytic viral DNA replication. PMID: 30021895
  9. Secreted Ta9 has therefore, not only the ability to stimulate CD8+ T cells, but also the potential to activate AP-1-driven transcription and contribute to T. annulata-induced leukocyte transformation PMID: 29738531
  10. MiR-216b directly targets c-Jun, thereby reducing AP-1-dependent transcription and sensitizing cells to ER stress-dependent apoptosis. PMID: 27173017
  11. results suggest that c-Jun, p38 MAPK, PIK3CA/Akt, and GSK3 signaling involved in the effect of miR-203 on the proliferation of hepatocellular carcinoma cells. PMID: 28887744
  12. These findings suggest that increased JUN expression and activity may contribute to gefitinib resistance in non-small cell lung cancer. PMID: 28566434
  13. the results indicated that butein has antiproliferative and proapoptotic properties through the suppression of NF-kappaB, AP-1 and Akt signaling in HTLV-1-infected T cells, both in vitro and in vivo, suggesting its therapeutic potential against HTLV-1-associated diseases including adult T-cell leukemia/lymphoma PMID: 28586006
  14. Results show that VEGFA induces c-jun expression in mediating human retinal microvascular endothelial cell migration, sprouting and tube formation, and that Pyk2-STAT3 signaling enhances cJun expression in the mediation of retinal neovascularization. PMID: 27210483
  15. Increased c-jun expression is associated with nasopharyngeal carcinoma. PMID: 28269757
  16. thrombin binding to PAR-1 receptor activated Gi-protein/c-Src/Pyk2/EGFR/PI3K/Akt/p42/p44 MAPK cascade, which in turn elicited AP-1 activation and ultimately evoked MMP-9 expression and cell migration in SK-N-SH cells. PMID: 27181591
  17. Findings provide evidence that phospho-c-Jun activates an important regulatory mechanism to control DNMT1 expression and regulate global DNA methylation in glioblastoma. PMID: 28036297
  18. results demonstrated for the first time the regulatory mechanism of miR-744 transcription by c-Jun, providing a potential mechanism underlying the upregulation of miR-744 in cancers PMID: 27533465
  19. Results provide evidence that NuRD represses c-Jun transcription directly which, in the absence of MBD3, activates endogenous pluripotent genes and regulates induced cancer stem cells-related genes. PMID: 27894081
  20. Taken together, these results indicated that PAR1 signalingmediated cJun activation promotes early apoptosis of HUVEC cells induced by heat stress. PMID: 28447716
  21. Cheliensisin A (Chel A)treatment led to PH domain and Leucine rich repeat Protein Phosphatases (PHLPP2) protein degradation and subsequently increased in c-Jun phosphorylation, which could be attenuated by inhibition of autophagy mediated by Beclin 1. PMID: 27556506
  22. The positive feedback regulation of OCT4 and c-JUN, resulting in the continuous expression of oncogenes such as c-JUN, seems to play a critical role in the determination of the cell fate decision from induced pluripotent stem cells to cancer stem cells in liver cancer. PMID: 27341307
  23. miR-26b plays an anti-metastatic role and is downregulated in gastric cancer tissues via the KPNA2/c-jun pathway PMID: 27078844
  24. The IL1B/AP-1/miR-30a/ADAMTS-5 axis regulates cartilage matrix degradation in osteoarthritis. PMID: 27067395
  25. TGM2 is involved in amyloid-beta (1-42)-induced pro-inflammatory activation via AP1/JNK signaling pathways in cultured monocytes. PMID: 27864692
  26. Integrative genomic analysis indicated overexpression of the AP-1 transcriptional complex suggesting experimental therapeutic rationales, including blockade of the renin-angiotensin system. This led to the repurposing of the angiotensin II receptor antagonist, irbesartan, as an anticancer therapy, resulting in the patient experiencing a dramatic and durable response. PMID: 27022066
  27. Knockdown of CD44 reduced the protein level of xCT, a cystine transporter, and increased oxidative stress. However, an increase in GSH was also observed and was associated with enhanced chemoresistance in CD44-knockdown cells. Increased GSH was mediated by the Nrf2/AP-1-induced upregulation of GCLC, a subunit of the enzyme catalyzing GSH synthesis PMID: 28185919
  28. study highlights the role of AP1 in promoting the host gene expression profile that defines Ebola virus pathogenesis. PMID: 28931675
  29. This is the first study to show how TGF-beta regulates the expression of Claudin-4 through c-Jun signaling and how this pathway contributes to the migratory and tumorigenic phenotype of lung tumor cells. PMID: 27424491
  30. Data show that BRD4 controls RUNX2 by binding to the enhancers (ENHs) and each RUNX2 ENH is potentially controlled by a distinct set of TFs and c-JUN as the principal pivot of this regulatory platform. PMID: 28981843
  31. AP-1 likely plays a more important role in the AR cistrome in fibroblasts. PMID: 27634452
  32. elevated levels of bile acid increase the tumorigenic potential of pancreatic cancer cells by inducing FXR/FAK/c-Jun axis to upregulate MUC4 expression. PMID: 27185392
  33. Immunohistochemistry was employed to analyze cFos, cJun and CD147 expression in 41 UCB cases and 34 noncancerous human bladder tissues. PMID: 28358415
  34. Taken together, these findings indicate that LT reduces c-Jun protein levels via two distinct mechanisms, thereby inhibiting critical cell functions, including cellular proliferation. PMID: 28893904
  35. Expression of either dominant-negative or constitutively active mutants of Nrf2, ATF4, or c-Jun confirmed that distinct transcription units are regulated by these transcription factors. PMID: 27278863
  36. mutually exclusive transcriptional regulation by AP-1 (cjun/cfos) and non-canonical NF-kappaB (RelB/p52) downstream of MEK-ERK and NIK-IKK-alpha-NF-kappaB2 (p100) phosphorylation, respectively was responsible for persistent Ccl20 expression in the colonic cells. PMID: 27590109
  37. Glucocorticoid receptor (GR) is recruited to activator protein-1 (AP-1) target genes in a DNA-binding-dependent manner. PMID: 28591827
  38. These results suggested that hyperphosphatemia in the patients with CKD suppresses bone resorption by inhibiting osteoclastogenesis, and this impairs the regulation of bone metabolism. PMID: 28939042
  39. These results suggest that Bacteroides fragilis enterotoxin induced accumulation of autophagosomes in endothelial cells, but activation of a signaling pathway involving JNK, AP-1, and CHOP may interfere with complete autophagy. PMID: 28694294
  40. Overall, our results suggest that miR-4632 plays an important role in regulating HPASMC proliferation and apoptosis by suppression of cJUN, providing a novel therapeutic miRNA candidate for the treatment of pulmonary vascular remodeling diseases. It also implies that serum miR-4632 has the potential to serve as a circulating biomarker for PAH diagnosis. PMID: 28701355
  41. Findings suggest that AP-1 factors are regulators of RNA polymerase III (Pol III)-driven 5S rRNA and U6 snRNA expression with a potential role in cell proliferation. PMID: 28488757
  42. Our results indicate that assessing AP1 and PEA3 transcription factor status might be a good indicator of OAC status. However, we could not detect any associations with disease stage or patient treatment regime. This suggests that the PEA3-AP1 regulatory module more likely contributes more generally to the cancer phenotype. In keeping with this observation, depletion of ETV1 and/or ETV4 causes an OAC cell growth defect PMID: 28859074
  43. shRNA-mediated inhibition of JUN decreases AML cell survival and propagation in vivo. These data uncover a previously unrecognized role of JUN as a regulator of the unfolded protein response PMID: 27840425
  44. These findings demonstrate an essential role for the ERK pathway together with c-JUN and c-FOS in the differentiation activity of LukS-PV. PMID: 27102414
  45. The present study defines the minimal TIM-3 promoter region and demonstrates its interaction with c-Jun during TIM-3 transcription in CD4(+) T cells. PMID: 27243212
  46. Taken together, our data demonstrate that JNK regulates triple-negative breast cancer (TNBC)tumorigenesis by promoting CSC phenotype through Notch1 signaling via activation of c-Jun and indicate that JNK/c-Jun/Notch1 signaling is a potential therapeutic target for TNBC PMID: 27941886
  47. Regulation of osteosarcoma cell lung metastasis by the c-Fos/AP-1 target FGFR1 PMID: 26387545
  48. c-jun promoted FOXK1-mediated proliferation and metastasis via orthotopic implantation. PMID: 27882939
  49. Data provide evidence that AP-1 is a key determinant of endocrine resistance of breast cancer cells by mediating a global shift in the estrogen receptor transcriptional program. PMID: 26965145
  50. Comparison of how AP-1 (Jun/Jun dimer) and Epstein-Barr virus Zta recognize methyl groups within their cognate response elements PMID: 28158710

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Subcellular Location Nucleus
Protein Families BZIP family, Jun subfamily
Database Links

HGNC: 6204

OMIM: 165160

KEGG: hsa:3725

STRING: 9606.ENSP00000360266

UniGene: Hs.696684

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