Recombinant Human c-JUN Protein

Name: Recombinant Human c-JUN Protein
Brand: Beta LifeScience
SKU: BL-1091SG
Availability: InStock

Collections: All products, High-quality recombinant proteins, Other recombinant proteins

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Product Overview

Tag	GST
Host Species	Human
Accession	NM_002228
Synonym	AP1
Background	c-Jun is a proto-oncogene that forms a complex with c-Fos which regulates transcription from promoters containing AP-1 activation elements (1). c-Jun has specific DNA binding activity and following in vitro translation, c-Jun binds as a homodimer to the AP-1 DNA site. The transactivating function of c-Jun is acutely regulated by a wide variety of cellular signals via modulation of phosphorylation of two serines (63 and 73). Jun N-terminal domain kinases (JNKs), are responsible for mediating S63/73 phosphorylation on c-Jun in response to a variety of cellular stimuli including TNF-a, heat stress and u.v. light (2).
Description	Recombinant human c-JUN (1-79) was produced in E. coli using a N-terminual GST tag. This protein is purified with our unique purification methods.
Source	E.coli
AA Sequence	1-79
Molecular Weight	~35 kDa
Purity	For specific purity information on a given lot, see related COA.
Endotoxin	< 1.0 EU per μg of the protein as determined by the LAL method
Formulation	Recombinant protein is supplied in 50mM Tris-HCl, pH 7.5, 50mM NaCl, 10mM Glutathione, 0.25mM DTT, 0.1mM EDTA, 0.1mM PMSF and 25% glycerol.
Stability	The recombinant protein is stable for up to 12 months at -70°C
Usage	For Research Use Only
Storage	Recombinant Human c-JUN Protein should be stored should be stored at < -70°C. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.

Target Details

Target 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. Binds to the USP28 promoter in colorectal cancer (CRC) cells.
Subcellular Location	Nucleus.
Protein Families	BZIP family, Jun subfamily
Database References	HGNC: 6204 OMIM: 165160 KEGG: hsa:3725 STRING: 9606.ENSP00000360266 UniGene: PMID: 29440459 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 a novel cascade mediated by AP-1 and FOXF1 that regulates oncogene-induced senescence, is reported. PMID: 30119690 Multivalent Interactions with Fbw7 and Pin1 Facilitate Recognition of c-Jun by the Fbw7. PMID: 29225075 High AP-1 expression is associated with metastasis in colon cancer. PMID: 29305742 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 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 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 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 MiR-216b directly targets c-Jun, thereby reducing AP-1-dependent transcription and sensitizing cells to ER stress-dependent apoptosis. PMID: 27173017 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 These findings suggest that increased JUN expression and activity may contribute to gefitinib resistance in non-small cell lung cancer. PMID: 28566434 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 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 Increased c-jun expression is associated with nasopharyngeal carcinoma. PMID: 28269757 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 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 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 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 Taken together, these results indicated that PAR1 signalingmediated cJun activation promotes early apoptosis of HUVEC cells induced by heat stress. PMID: 28447716 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 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 miR-26b plays an anti-metastatic role and is downregulated in gastric cancer tissues via the KPNA2/c-jun pathway PMID: 27078844 The IL1B/AP-1/miR-30a/ADAMTS-5 axis regulates cartilage matrix degradation in osteoarthritis. PMID: 27067395 TGM2 is involved in amyloid-beta (1-42)-induced pro-inflammatory activation via AP1/JNK signaling pathways in cultured monocytes. PMID: 27864692 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 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 study highlights the role of AP1 in promoting the host gene expression profile that defines Ebola virus pathogenesis. PMID: 28931675 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 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 AP-1 likely plays a more important role in the AR cistrome in fibroblasts. PMID: 27634452 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 Immunohistochemistry was employed to analyze cFos, cJun and CD147 expression in 41 UCB cases and 34 noncancerous human bladder tissues. PMID: 28358415 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 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 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 Glucocorticoid receptor (GR) is recruited to activator protein-1 (AP-1) target genes in a DNA-binding-dependent manner. PMID: 28591827 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 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 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 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 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 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 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 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 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 Regulation of osteosarcoma cell lung metastasis by the c-Fos/AP-1 target FGFR1 PMID: 26387545 c-jun promoted FOXK1-mediated proliferation and metastasis via orthotopic implantation. PMID: 27882939 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 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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Proteins are sensitive to heat, and freeze-drying can preserve the activity of the majority of proteins. It improves protein stability, extends storage time, and reduces shipping costs. However, freeze-drying can also lead to the loss of the active portion of the protein and cause aggregation and denaturation issues. Nonetheless, these adverse effects can be minimized by incorporating protective agents such as stabilizers, additives, and excipients, and by carefully controlling various lyophilization conditions.

Commonly used protectant include saccharides, polyols, polymers, surfactants, some proteins and amino acids etc. We usually add 8% (mass ratio by volume) of trehalose and mannitol as lyoprotectant. Trehalose can significantly prevent the alter of the protein secondary structure, the extension and aggregation of proteins during freeze-drying process; mannitol is also a universal applied protectant and fillers, which can reduce the aggregation of certain proteins after lyophilization.

Our protein products do not contain carrier protein or other additives (such as bovine serum albumin (BSA), human serum albumin (HSA) and sucrose, etc., and when lyophilized with the solution with the lowest salt content, they often cannot form A white grid structure, but a small amount of protein is deposited in the tube during the freeze-drying process, forming a thin or invisible transparent protein layer.

Reminder: Before opening the tube cap, we recommend that you quickly centrifuge for 20-30 seconds in a small centrifuge, so that the protein attached to the tube cap or the tube wall can be aggregated at the bottom of the tube. Our quality control procedures ensure that each tube contains the correct amount of protein, and although sometimes you can't see the protein powder, the amount of protein in the tube is still very precise.

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