AKIRIN1

Last update 08 May 2025

Basic Info

Synonyms

akirin 1, Akirin-1, AKIRIN1

+ [2]

Introduction

Molecular adapter that acts as a bridge between proteins, and which is involved skeletal muscle development (By similarity). Functions as a signal transducer for MSTN during skeletal muscle regeneration and myogenesis (By similarity). May regulate chemotaxis of both macrophages and myoblasts by reorganising actin cytoskeleton, leading to more efficient lamellipodia formation via a PI3 kinase dependent pathway (By similarity). In contrast to AKIRIN2, not involved in nuclear import of proteasomes (PubMed:34711951).

100 Clinical Results associated with AKIRIN1

100 Translational Medicine associated with AKIRIN1

0 Patents (Medical) associated with AKIRIN1

Literatures (Medical) associated with AKIRIN1

01 Jun 2024·Smart Medicine

Roles of Akirin1 in early prediction and treatment of graft kidney ischemia‒reperfusion injury

Article

Author: Li, Yang ; Zhou, Xiang ; Li, Li ; Shi, Wei ; He, Weiyang ; Li, Xinyuan ; Chen, Guo ; Peng, Xiang ; Feng, Zhenwei ; Chen, Daihui ; Yu, Haitao ; Li, Jie ; Li, Mao ; Zhang, Chunlin ; Mei, Yuhua ; Gou, Xin ; Liang, Simin

AbstractFerroptosis is a predominant contributor to graft kidney ischemia‒reperfusion injury (IRI), resulting in delayed graft function (DGF). However, much less is known about the early predicting biomarkers and therapeutic targets of DGF, especially aiming at ferroptosis. Here, we propose a precise predicting model for DGF, relying on the Akirin1 level in extracellular vesicles (EVs) derived from recipient urine 48 h after kidney transplant. In addition, we decipher a new molecular mechanism whereby Akirin1 induces ferroptosis by strengthening TP53‐mediated suppression of SLC7A11 during the graft kidney IRI process, that is, Akirin1 activates the EGR1/TP53 axis and inhibits MDM2‐mediated TP53 ubiquitination, accordingly upregulating TP53 in two ways. Meanwhile, we present the first evidence that miR‐136‐5p enriched in EVs secreted by human umbilical cord mesenchymal stem cells (UM‐EVs) confers robust protection against ferroptosis and graft kidney IRI by targeted inhibition of Akirin1 but knockout of miR‐136‐5p in UM sharply mitigates the protection of UM‐EVs. The functional and mechanistic regulation of Akirin1 is further corroborated in an allograft kidney transplant model in wild‐type and Akirin1‐knockout mice. In summary, these findings suggest that Akirin1, which prominently induces ferroptosis, is a pivotal biomarker and target for early diagnosis and treatment of graft kidney IRI and DGF after kidney transplant.

01 Mar 2022·iScienceQ2 · CROSS-FIELD

Identification of new ETV6 modulators through a high-throughput functional screening

Q2 · CROSS-FIELD

ArticleOA

Author: Caron, Maxime ; Neveu, Benjamin ; Cassart, Pauline ; St-Onge, Pascal ; Richer, Chantal ; Sinnett, Daniel ; Gobeil, Stéphane ; Jimenez-Cortes, Camille ; Fuchs, Claire ; Garnier, Nicolas

ETV6 transcriptional activity is critical for proper blood cell development in the bone marrow. Despite the accumulating body of evidence linking ETV6 malfunction to hematological malignancies, its regulatory network remains unclear. To uncover genes that modulate ETV6 repressive transcriptional activity, we performed a specifically designed, unbiased genome-wide shRNA screen in pre-B acute lymphoblastic leukemia cells. Following an extensive validation process, we identified 13 shRNAs inducing overexpression of ETV6 transcriptional target genes. We showed that the silencing of AKIRIN1, COMMD9, DYRK4, JUNB, and SRP72 led to an abrogation of ETV6 repressive activity. We identified critical modulators of the ETV6 function which could participate in cellular transformation through the ETV6 transcriptional network.

01 Nov 2020·Cellular and Molecular Life SciencesQ2 · BIOLOGY

Akirin proteins in development and disease: critical roles and mechanisms of action

Q2 · BIOLOGY

Review

Author: Smolikove, Sarit ; Weiner, Joshua A ; Bosch, Peter J ; Peek, Stacey L

The Akirin genes, which encode small, nuclear proteins, were first characterized in 2008 in Drosophila and rodents. Early studies demonstrated important roles in immune responses and tumorigenesis, which subsequent work found to be highly conserved. More recently, a multiplicity of Akirin functions, and the associated molecular mechanisms involved, have been uncovered. Here, we comprehensively review what is known about invertebrate Akirin and its two vertebrate homologues Akirin1 and Akirin2, highlighting their role in regulating gene expression changes across a number of biological systems. We detail essential roles for Akirin family proteins in the development of the brain, limb, and muscle, in meiosis, and in tumorigenesis, emphasizing associated signaling pathways. We describe data supporting the hypothesis that Akirins act as a "bridge" between a variety of transcription factors and major chromatin remodeling complexes, and discuss several important questions remaining to be addressed. In little more than a decade, Akirin proteins have gone from being completely unknown to being increasingly recognized as evolutionarily conserved mediators of gene expression programs essential for the formation and function of animals.

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AKIRIN1

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