JUN

Case study 1: Nicholas Polakowski, 2020

HBZ is expressed by the complex retrovirus, Human T-cell Leukemia Virus type 1, and implicated in pathological effects associated with viral infection. From the nucleus, HBZ alters gene expression by interacting with a variety of transcriptional regulatory proteins, among which is c-Jun. Previously, one of the three HBZ variants, HBZUS, was reported to decrease c-Jun expression by promoting its degradation. Here the researchers show that another variant, HBZS1, produces the opposite effect. In the presence of HBZS1, c-Jun expression increases due to its stabilization. Our data suggest that this effect requires the ability of HBZS1 to interact with c-Jun. They provide evidence that HBZS1 inhibits the proteosomal degradation of c-Jun initiated by the Cop1-containing ubiquitin ligase complex. HBZS1 is the most abundant variant in HTLV-1-infected T-cells, and the data indicate that levels of c-Jun expression in infected cells are consistent with effects of HBZS1.

Fig1. Ectopically-expressed c-Jun was immunoprecipitated from MG132-treated HEK293T cells transfected with expression vectors for the indicated plasmids.

Fig2. Ectopic wild-type and mutant c-Jun levels were analyzed by western blot, probing the C-terminal Flag tag, from 20 μg of protein in whole cell extracts prepared from transiently-transfected HEK293T cells.

Case study 2: Luigi Mazzeo, 2024

There are significant commonalities among several pathologies involving fibroblasts, ranging from auto-immune diseases to fibrosis and cancer. Early steps in cancer development and progression are closely linked to fibroblast senescence and transformation into tumor-promoting cancer-associated fibroblasts (CAFs), suppressed by the androgen receptor (AR). Here, the researchers identify ANKRD1 as a mesenchymal-specific transcriptional coregulator under direct AR negative control in human dermal fibroblasts (HDFs) and a key driver of CAF conversion, independent of cellular senescence. ANKRD1 expression in CAFs is associated with poor survival in HNSCC, lung, and cervical SCC patients, and controls a specific gene expression program of myofibroblast CAFs (my-CAFs). ANKRD1 binds to the regulatory region of my-CAF effector genes in concert with AP-1 transcription factors, and promotes c-JUN and FOS association. Targeting ANKRD1 disrupts AP-1 complex formation, reverses CAF activation, and blocks the pro-tumorigenic properties of CAFs in an orthotopic skin cancer model. ANKRD1 thus represents a target for fibroblast-directed therapy in cancer and potentially beyond.

Fig3. In vitro protein interactions. Glutathione-conjugated beads were used to immunoprecipitate GST-tagged ANKRD1 (100 ng) recombinant protein mixed with the following recombinant proteins.

Fig4. Immunoprecipitation assays (IP) with anti-V5 (ANKRD1) or nonimmune (IgG) antibodies from HEK293 cells lysates infected with ANKRD1OE vector followed by immunoblotting for ANKRD1, JUN, and FRA2.

JUN involved in several pathways and played different roles in them. We selected most pathways JUN participated on our site, such as AGE/RAGE pathway, ATF-2 transcription factor network, Activated TLR4 signalling, which may be useful for your reference. Also, other proteins which involved in the same pathway with JUN were listed below. Creative BioMart supplied nearly all the proteins listed, you can search them on our site.

JUN has several biochemical functions, for example, DNA binding, GTPase activator activity, HMG box domain binding. Some of the functions are cooperated with other proteins, some of the functions could acted by JUN itself. We selected most functions JUN had, and list some proteins which have the same functions with JUN. You can find most of the proteins on our site.

JUN has direct interactions with proteins and molecules. Those interactions were detected by several methods such as yeast two hybrid, co-IP, pull-down and so on. We selected proteins and molecules interacted with JUN here. Most of them are supplied by our site. Hope this information will be useful for your research of JUN.

FOS

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