Drug Target and Biomarker: c-Jun (G3725)

Target Name: JUN

NCBI ID: G3725

Drug Target and Biomarker: c-Jun

CEH (compound name not provided) can reverse multidrug resistance (MDR) in esophageal squamous cell carcinoma (ESCC) through the activation of the c-Jun/JNK and P53 signaling pathways. Inhibitors of JNK and p53 can also restore the reversion of MDR mediated by CEH.
Activation of the c-Jun/JNK signaling pathway is involved in the reversal of MDR in ESCC mediated by CEH, indicating that CEH may have potential as a novel drug for cancer chemotherapy.
The activation of c-Jun, along with other transcription factors like cFos, plays a role in increased interleukin-6 (IL-6) gene transcription in immature enterocytes. However, the expression of JunD during enterocyte development can replace the activating cJun/cJun or cJun/cFos dimers with less potent JunD/cJun or JunD/cFos dimers, leading to lower IL-6 gene transcription.
USP28, an oncoprotein, stabilizes several proteins involved in proliferation, cell cycle progression, and oncogenesis, including c-Jun. It also stabilizes the Np63 transcription factor, which regulates SCC (squamous cell carcinoma) cell identity, oncogenesis, proliferation, cell cycle progression, and genomic stability.
Serine stress induced by serum deprivation can lead to the upregulation of c-Jun phosphorylation, which then activates the AP1 transcription factor and initiates viral transcription of HIV-1 in latently infected monocytes.
The expression of ABCB1, a transporter associated with multidrug resistance, is partly dependent on c-Jun. CHD1L expression can increase both c-Jun and ABCB1 levels, and silencing c-Jun blocks the increased transcriptional activity and expression of ABCB1 induced by CHD1L in non-small cell lung cancer cells.

Please note that the references provided in the summary are labeled with numbers,,,, and to indicate the source of each viewpoint.
Based on the given context information, here are some key viewpoints about JUN (also referred to as cJun and c-JUN):

JNK-dependent hyperphosphorylation of cJun inhibits gene activation and migration by Jun/Fos dimers.
Interacting with SIRT1, c-JUN is targeted for deacetylation and inhibition, exerting inhibitory effects on ARHGAP5.
The AP1 subunit is involved in assembling the CPAC machinery, which activates NLRP3 expression in OA cells.
JUN, JUNB, FOS, and FOSL1 form an AP-1 complex and regulate gene expression.
In T-ALL, inactivation of the KLF4 gene leads to the activation of downstream targets such as JNK and c-Jun, promoting cell proliferation and self-renewal.

Protein Name: Jun Proto-oncogene, AP-1 Transcription Factor Subunit

Functions: Transcription factor that recognizes and binds to the AP-1 consensus motif 5'-TGA[GC]TCA-3' (PubMed:10995748, PubMed:22083952). Heterodimerizes with proteins of the FOS family to form an AP-1 transcription complex, thereby enhancing its DNA binding activity to the AP-1 consensus sequence 5'-TGA[GC]TCA-3' and enhancing its transcriptional activity (By similarity). Together with FOSB, plays a role in activation-induced cell death of T cells by binding to the AP-1 promoter site of FASLG/CD95L, and inducing its transcription in response to activation of the TCR/CD3 signaling pathway (PubMed:12618758). Promotes activity of NR5A1 when phosphorylated by HIPK3 leading to increased steroidogenic gene expression upon cAMP signaling pathway stimulation (PubMed:17210646). Involved in activated KRAS-mediated transcriptional activation of USP28 in colorectal cancer (CRC) cells (PubMed:24623306). Binds to the USP28 promoter in colorectal cancer (CRC) cells (PubMed:24623306)

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