EGR1 (Early Growth Response 1)

We developed a viable in vitro model to study contact-compression, showing biomechanical inflammatory and remodeling responses. With adjustable components, this model can be applied to further study tissue responses to lung implants.

Rescue experiments confirmed that wild-type GAS6, but not the truncated variant, restored cellular function. These findings establish GAS6 as a critical regulator of neuro-glial homeostasis and identify its deficiency as the cause of a previously unreported childhood-onset demyelinating disease.

This article was published in Volume 67, issue 4 of publishing year 2023, with a mistake in Figure 3. The correct Figure 3 is the one included in this erratum.

Transcriptomic analysis identifies Egr1 as a putative master regulator of murine hematopoietic stem and progenitor cell aging, demonstrating PURE-seq's utility as a discovery platform for basic science applications. PURE-seq offers a simple and highly sensitive method for single-cell sequencing ultra-rare cells.

Based on molecular docking and molecular dynamics results, NEDD4L is believed to be a 18β-GRA biomarker, while sodium channel protein type 5 subunit alpha (SCN5A) and early growth response protein 1 (EGR1) are the potential upstream and downstream regulatory proteins, respectively. These findings provide a theoretical basis for future experimental verification.

The obtained results can guide the design of new experiments studying the role of apoptosis in carcinogenesis and aid in the search for novel therapeutic targets and approaches for HCC therapy using apoptosis modulation in malignant hepatocytes. Furthermore, the proposed approach to reconstructing and analyzing the apoptosis regulation gene network in hepatocellular carcinoma can be applied to analyze other tumor forms providing a systemic understanding of disturbances in key regulatory processes in oncogenesis and potential therapy targets.

However, on this basis, knocking down EGR1 restored the anti-cancer effect conferred by overexpression of LIPT1. This work aimed to investigate the transcriptional activation of LIPT1 by EGR1 in RCC98 cells to repress the malignant progression of cancer cells while enhancing the sensitivity of RCC98 cells to cuproptosis.

Non-neuronal cell types including astrocytes, oligodendrocytes, and vascular cells also exhibited region-specific translational changes in neurotransmitter transport, lipid synthesis, myelination, and stress response pathways, some of which co-varied with regional neuron state. Together, our study reveals brain-wide translation dysregulation as a critical mechanism underlying SCZ pathophysiology.

EGR1 activates RRN3 gene transcription by binding to the RRN3 gene promoter. Thus, EGR1 promotes Pol Ⅰ-directed transcription and cancer cell growth by both interacting with Pol I machinery factors and controlling RRN3 expression.

In vivo dissection of the RNF126-MIDN axis shows that it governs EGR1 abundance and, consequently, the tumor-suppressor proteins PTEN and p53, thereby restraining the progression of testicular germ-cell tumors (TGCTs). Our findings reveal an unappreciated layer of MIDN regulation and identify the RNF126-MIDN ubiquitination cascade as a potential therapeutic vulnerability in TGCTs and related malignancies.

In conclusion, these findings suggest that MLN4924 exerts an anti-tumor effect on AML by inducing apoptosis through the ROS-EGR1-BTG2 signaling axis. Our research provides a novel theoretical basis for the clinical potential of MLN4924 in improving the treatment of AML patients, offers novel strategies for AML treatment, and thereby advances the implementation of precision medicine.

Furthermore, fisetin was identified as an anti-senescence drug for mitigating B cell senescence and enhancing NICB efficacy. Our findings highlight the role of senescent EGR1+ B cells in ESCC immunotherapy failure and suggest targeting B cell senescence as a strategy to improve NICB outcomes.