Transcription factor Jun is a protein that in humans is encoded by the JUN gene. c-Jun, in combination with protein c-Fos, forms the AP-1 early response transcription factor.

Apr 18, 2016 · Here we report that the transcription factor c-Jun, product of the proto-oncogene JUN, is a key regulator of mitochondrial glutaminase (GLS) levels. Activation of c-Jun downstream of...

Nov 30, 2018 · Jun -deleted samples, found in 17–23% of luminal patients, had significantly higher Myc signature scores that predicted worse survival. Entinostat inhibited luminal breast cancer through Myc signaling, which was upregulated by Jun DNA loss to promote resistance to entinostat in our models.

Aug 19, 2024 · The present study shows for the first time that MYC and JUNB, two crucial TFs implicated in MM pathogenesis, orchestrate distinct transcriptional programs.

Feb 6, 2004 · This region of c-Myc shares homology with the delta domain of c-Jun, which is required for JNK association and subsequent targeting of c-Jun for ubiquitination under non-stressed growth conditions. Here we demonstrate that JNK associates with, and mediates, c-Myc ubiquitination and degradation.

These results reveal that DYRK2 regulates tumor progression through modulation of c-Jun and c-Myc. The c-Jun and c-Myc transcription factors are critical promoters of cellular proliferation. Dysregulated expression and activation of these oncogenes are frequently observed in most human cancers.

JunD, a member of the AP-1 family, is essential for cell proliferation in prostate cancer (PCa) cells. We recently demonstrated that JunD knock-down (KD) in PCa cells results in cell cycle arrest in G 1 -phase concomitant with a decrease in cyclin D1, …

JUN, MYC, and VEGFA are abnormally elevated in the synovial tissue of OA patients and correlated with disease severity. To investigate the differential mRNA expression of JUN, MYC, and VEGFA in OA, we examined synovial tissues from 20 OA patients and 10 healthy controls.

Oct 31, 2023 · Transcription factors are critical components of signal transduction pathways that can transmit a regulatory signal to altered patterns of gene expression. It is not surprising that the disruption of normal regulation of such important control points can contribute to tumorigenesis.

Downregulation of DYRK2 correlated with high levels of unphosphorylated c-Jun and c-Myc and, importantly, with invasiveness of human breast cancers. These results reveal that DYRK2 regulates tumor progression through modulation of c-Jun and c-Myc.