Other Name(s): AP-1, AP1, c-Jun, cJun, c-JUN
Drug Target Analysis Report Drug Target Analysis Report Content

About the Target

Based on the provided context information, some key viewpoints related to the keyword "c-Jun" can be summarized as follows:

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 [1].
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 [1].
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 [2].
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 [3].
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 [4].
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 [5].

Please note that the references provided in the summary are labeled with numbers [1], [2], [3], [4], and [5] 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 [6].
Interacting with SIRT1, c-JUN is targeted for deacetylation and inhibition, exerting inhibitory effects on ARHGAP5 [7].
The AP1 subunit is involved in assembling the CPAC machinery, which activates NLRP3 expression in OA cells [8].
JUN, JUNB, FOS, and FOSL1 form an AP-1 complex and regulate gene expression [9].
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 [10].

These viewpoints provide an understanding of how JUN is involved in gene expression regulation, migration inhibition, deacetylation-mediated effects, OA pathogenesis, and T-ALL leukemogenesis.

Figure [1]

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Note: If you are interested in the full version of this target analysis report, or if you'd like to learn how our AI-powered BDE-Chem can design therapeutic molecules to interact with the JUN target at a cost 90% lower than traditional approaches, please feel free to contact us at BD@silexon.ai.

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