ID3 (Inhibitor Of DNA Binding 3, HLH Protein)

Primary human VSMCs from subjects with the rs11574 minor allele exhibited reduced mitogen-stimulated proliferation. Taken together, these results provide the first characterization of altered molecular and cellular functions of this disease-associated SNP in ID3 at rs11574.

Targeted topical AAV5-Id3 gene therapy is tolerable, safe, and nontoxic to the eyes in vivo. Topical AAV5-Id3 gene therapy treats corneal fibrosis without significant side effects in vivo.

The risk model constructed in this study effectively predicts the prognosis of LUAD patients. PLEK2 is highly expressed in LUAD and associated with EGFR-TKIs resistance, suggesting its potential as a prognostic biomarker and therapeutic target.

IU1 not only impedes tumor cell proliferation, but also augments the efficacy of PD-L1 monoclonal antibody therapy by enhancing anti-tumor immune responses. These findings elucidate a novel mechanism by which the USP35-ID3-PD-L1 axis contributes to immune evasion in CRC and propose a potential therapeutic strategy to improve the efficacy of immunotherapy in CRC patients.

We further discuss the theory that aberrant activation-induced cytidine deaminase (AID) expression, in the setting of EBV infection and chronic malaria exposure, is the most likely aetiology of endemic BL. This review provides a comprehensive summary of key molecular differences between EBV-positive and EBV-negative BL, that may guide the development of future targeted therapeutic strategies.

TGF-β and retinoic acid were required for formation and survival of TCF1- and ID3-expressing TRM cells and restrained their differentiation into CX3CR1+ effector cells during reinfection. Thus, stem-like cells control the quality and recall capacity of TRM cells, thereby contributing to anamnestic memory responses.

In conclusion, molecular testing enables a subset of HGBCL-NOS to be assigned to established categories. Based on rarity and diagnostic challenges, broader inclusion of HGBCL-NOS should be considered in biomarker-driven DLBCL trials.

Our study reveals that SMYD2 is an important epigenetic mediator that activates BMP4/R-SMADs/ID3 axis, leading to enhanced stemness and sorafenib resistance. Thus, SMYD2 might represent a potential biomarker and future epigenetic therapeutic target for sorafenib resistance of HCC.

These findings shed light on the complex transcriptional network regulating TSPAN32 and its dysregulation in BL. Overall, our study suggests that TSPAN32 may serve as both a biomarker and a potential therapeutic target for this disease.

The distinctive chromosomal change of HGBCL-11q,MYCR was the gain or amplification of 3q29. Our cohort of patients with HGBCL-11q,MYCR had similar relapse-free survival to that of patients with HGBCL-11q and BL, if treated with BL-directed regimens.

By integrating analysis of ChIP-seq, RNA-seq, and ImmPort gene sets, we found that ID3's DNA-assisted binding function was widespread and could either enhance or suppress gene transcription, not only affecting tumor immune escape through immune checkpoints but also regulating various cytokines and immune cells involved in tumor immunity. In conclusion, our study uncovers a mechanism by which ID3 promotes immune evasion in CRC and implicates that targeting ID3 may improve the efficacy of anti-PD-1/PD-L1 immunotherapy.

Based on rarity and diagnostic challenges, broader inclusion of HGBCL-NOS should be considered in biomarker-driven DLBCL trials. Molecular analyses reveal that HGBCL-NOS encompasses a heterogeneous collection of tumors.A subset of HGBCL-NOS can be assigned to established molecular groups, while others remain unclassified.