ABLIM2

Last update 08 May 2025

Basic Info

Synonyms

abLIM-2, ABLIM2, actin binding LIM protein family member 2

+ [3]

Introduction

May act as scaffold protein. May stimulate ABRA activity and ABRA-dependent SRF transcriptional activity.

100 Clinical Results associated with ABLIM2

100 Translational Medicine associated with ABLIM2

0 Patents (Medical) associated with ABLIM2

Literatures (Medical) associated with ABLIM2

02 Jan 2023·Expert Opinion on Drug Metabolism & Toxicology

Identification of genetic biomarkers associated with pharmacokinetics and pharmacodynamics of apixaban in Chinese healthy volunteers

Article

Author: Meng, Xianmin ; Cui, Yimin ; Zhao, Xia ; Xie, Qiufen ; Mu, Guangyan ; Liu, Zhiyan ; Wang, Zining ; Zhang, Fan ; Wang, Zhe ; Bao, Jiachun ; Song, Jinfang ; Jiang, Jie ; Zhou, Shuang ; Xiang, Qian ; Zhang, Hanxu ; Liao, Maoxing

BACKGROUNDApixaban is a superior direct oral anticoagulant exihibiting interindividual variability in concentration and response in the real world. The present study aimed to identify genetic biomarkers associated with pharmacokinetics (PK) and pharmacodynamics (PD) of apixaban in healthy Chinese subjects.METHODSThis multicenter study included 181 healthy Chinese adults taking a single dose of 2.5 mg or 5 mg apixaban and assessed their PK and PD parameters. Genome-wide single nucleotide polymorphism (SNP) genotyping was performed using the Affymetrix Axiom CBC_PMRA Array. Candidate gene association analysis and genome-wide association study were conducted to identify genes with a predictive value for PK and PD parameters of apixaban.RESULTSSeveral ABCG2 variants were associated with C_max and AUC_0-t of apixaban (p < 6.12 × 10^-5) and also presented significant differences of anti-Xa_3h activity and dPT_3h according to different ABCG2 genotypes (p < 0.05). Besides, ABLIM2 variants were found to be associated with PK characteristics and F13A1 and C3 variants were associated with PD characteristics of apixaban (p < 9.46 × 10^-8).CONCLUSIONABCG2 variants were found to be ideal genetic biomarkers for both PK and PD characteristics of apixaban. ABLIM2, F13A1 and C3 were identified as potential candidate genes associated with inter-individual variability of apixaban. This study was registered on ClinicalTrials.gov NCT03259399.

03 Oct 2022·Journal of Clinical Investigation

Relieving DYRK1A repression of MKL1 confers an adult-like phenotype to human infantile megakaryocytes

Article

Author: Sahu, Ranjit K ; Li, Hui ; Delehanty, Lorrie L ; Elagib, Kamaleldin E ; French, Deborah L ; Qin, Fujun ; Jobaliya, Chintan ; Shi, Xinrui ; Gadue, Paul ; Besson, Thierry ; Eto, Koji ; Cornelison, Robert ; Mosoyan, Goar ; Pacheco-Benichou, Alexandra ; Fruit, Corinne ; Goldfarb, Adam N ; Singh, Sandeep ; Brock, Ashton ; Iancu-Rubin, Camelia ; Morris, Stephan W ; Clementelli, Cara M

Infantile (fetal and neonatal) megakaryocytes (Mks) have a distinct phenotype consisting of hyperproliferation, limited morphogenesis, and low platelet production capacity. These properties contribute to clinical problems that include thrombocytopenia in neonates, delayed platelet engraftment in recipients of cord blood stem cell transplants, and inefficient ex vivo platelet production from pluripotent stem cell-derived Mks. The infantile phenotype results from deficiency of the actin-regulated coactivator, MKL1, which programs cytoskeletal changes driving morphogenesis. As a strategy to complement this molecular defect, we screened pathways with the potential to affect MKL1 function and found that DYRK1A inhibition dramatically enhanced Mk morphogenesis in vitro and in vivo. Dyrk1 inhibitors rescued enlargement, polyploidization, and thrombopoiesis in human neonatal Mks. Mks derived from induced pluripotent stem cells responded in a similar manner. Progenitors undergoing Dyrk1 inhibition demonstrated filamentous actin assembly, MKL1 nuclear translocation, and modulation of MKL1 target genes. Loss-of-function studies confirmed MKL1 involvement in this morphogenetic pathway. Expression of Ablim2, a stabilizer of filamentous actin, increased with Dyrk1 inhibition, and Ablim2 knockdown abrogated the actin, MKL1, and morphogenetic responses to Dyrk1 inhibition. These results delineate a pharmacologically tractable morphogenetic pathway whose manipulation may alleviate clinical problems associated with the limited thrombopoietic capacity of infantile Mks.

01 Mar 2022·Environmental Science and Pollution ResearchQ3 · ENVIRONMENTAL SCIENCE & ECOLOGY

Identification of epigenetic modifications mediating the antagonistic effect of selenium against cadmium-induced breast carcinogenesis

Q3 · ENVIRONMENTAL SCIENCE & ECOLOGY

Article

Author: Tang, Lu-Ying ; Wang, Qing ; Zhu, Rui-Mei ; Li, Ruo-Bi ; Li, Yue-Lin ; Jiang, Hong-Mei ; Zhang, Yi-Xin ; Ren, Ze-Fang ; Chen, Qian-Xin ; Liang, Zhuo-Zhi

The antagonistic effect of selenium (Se) against cadmium (Cd)-induced breast carcinogenesis was reported, but underlying mechanisms were unclear. The aim of this study was to identify the epigenetically regulated genes and biological pathways mediating the antagonistic effect. We exposed MCF-7 cells to Cd and Se alone or simultaneously. Cell proliferation was assessed by MTT assay, and differential epigenome (DNA methylation, microRNA, and long non-coding RNA) was obtained by microarrays. We cross-verified the epigenetic markers with differential transcriptome, and the ones modulated by Cd and Se in opposite directions were regarded to mediate the antagonistic effect. The epigenetically regulated genes were validated by using gene expression data in human breast tissues. We further assessed the biological functions of these validated genes. Our results showed that Se alleviated the proliferative effect of Cd on MCF-7 cell. A total of 10 epigenetically regulated genes were regarded to mediate the antagonistic effect, including APBA2, KIAA0895, DHX35, CPEB3, SVIL, MYLK, ZFYVE28, ABLIM2, GRB10, and PCDH9. Biological function analyses suggested that these epigenetically regulated genes were involved in multiple cancer-related pathways, such as focal adhesion and PI3K/Akt pathway. In conclusion, we provided evidence that Se antagonized the Cd-induced breast carcinogenesis via epigenetic modification and revealed the critical pathways.

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ABLIM2

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