Deltacoronavirus Modulates circRNA cGLIS3 Metabolism to Evade Host Antiviral Response. [PDF]
This study reveals that both deltacoronavirus nucleocapsid protein and host RNA binding protein IGF2BP2 promote circular RNA GLIS3 (cGLIS3) biogenesis by binding to GLIS3 pre‐mRNA. The m6A modification‐mediated cGLIS3‐IGF2BP2 interaction weakens RNase L‐mediated degradation of cGLIS3 while facilitates a ubiquitin‐dependent degradation of IGF2BP2, thus ...
Du L +10 more
europepmc +2 more sources
Targeting the NR1D1-IGF2BP2-V-ATPase Axis With Hybrid Nanovesicles Restores Macrophage Rhythms to Reverse Sepsis-Induced Immunosuppression. [PDF]
Sepsis disrupts immune‐cell rhythms and weakens bacterial clearance. Biomimetic nanovesicles combining erythrocyte and inflammation‐activated macrophage membranes deliver siNR1D1 to dysfunctional macrophages, restoring the NR1D1–IGF2BP2–V‐ATPase pathway, circadian regulation, phagolysosomal acidification, and antimicrobial defense.
Chen L +13 more
europepmc +2 more sources
ACSL4-Dependent Lysosomal Lipid Peroxidation Links WTAP-Mediated m<sup>6</sup>A Modification to Intervertebral Disc Degeneration. [PDF]
IL‐1β upregulates the protein level of WTAP, which promotes the m6A modification of ACSL4 mRNA in an IGF2BP2‐dependent manner, thereby enhancing its stability. The increased ACSL4 drives lipid peroxidation, leading to lysosomal membrane permeabilization (LMP) and impaired mitophagy, which collectively accelerate intervertebral disc degeneration (IVDD).
Jia S +8 more
europepmc +2 more sources
METTL3 Increases Temozolomide Resistance in MGMT-Negative Glioblastoma by Enhancing CBX5 mRNA Stability in an m<sup>6</sup>A-IGF2BP2-Dependent Manner. [PDF]
METTL3‐dependent m6A modification and IGF2BP2‐associated CBX5 mRNA stabilization help maintain CBX5 expression in MGMT‐negative glioblastoma. During temozolomide (TMZ) treatment, CBX5 contributes to ATM–RAD51‐associated signaling, limits persistent DNA damage and apoptosis, and thereby supports cell survival and TMZ resistance.
Deng H, Chen R, Qu D, Qu C, Shi J.
europepmc +2 more sources
The m6A reader IGF2BP2 promotes hepatocellular carcinoma progression via enhancing RELB stability [PDF]
N6-methyladenosine (m6A) modifications play a vital role in hepatocellular carcinoma (HCC) progression. However, the function of m6A reader proteins in HCC remains poorly understood. Here, we elucidate the role and mechanism of insulin-like growth factor
Hehua Ma +6 more
doaj +2 more sources
IGF2BP2 is a new identified N6‐methyladenosine (m6A) reader and associated with poor prognosis in many tumors. However, its role and related mechanism in breast cancer, especially in triple‐negative breast cancer (TNBC), remains unclear.
Qiang Ding, Tian Xia
exaly +2 more sources
O-GlcNAcylation of IGF2BP2 promotes angiogenesis after ischemic stroke by stabilizing PPP2CA in an m6A-dependent manner [PDF]
Background Angiogenesis is an important protective mechanism after ischemic stroke (IS). We aimed to investigate the effect of insulin like growth factor 2 mRNA binding protein 2 (IGF2BP2) O-GlcNAcylation in angiogenesis after IS.
Shengli Sun +4 more
doaj +2 more sources
Deficiency of the m6A reader IGF2BP2 mediates cellular senescence of chondrocytes and triggers cartilage degeneration [PDF]
Summary Accumulating evidence has identified N6-methyladenosine (m6A) regulation in the progression of age-related diseases. However, whether the m6A reader protein IGF2BP2 affects the occurrence of cartilage degeneration is still unknown.
Zhi-Han Shen +9 more
doaj +2 more sources
IGF2BP2 Overexpression Predicts Poor Prognosis and Correlates with PD-L1 Expression in Intrahepatic Cholangiocarcinoma [PDF]
Background: The immunologically cold nature and immunosuppressive tumor microenvironment (TME) of intrahepatic cholangiocarcinoma (ICC) contribute to its poor prognosis.
Jianan Shen +7 more
doaj +2 more sources
Objective: Investigation of the regulatory mechanisms of cell stemness in cholangiocarcinoma (CCA) is essential for developing effective therapies to improve patient outcomes.
Hua Ye +7 more
doaj +1 more source

