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Last update 08 May 2025

DUSP22

Last update 08 May 2025

Basic Info

Synonyms

dual specificity phosphatase 22, Dual specificity protein phosphatase 22, DUSP22

+ [12]

Introduction

Dual specificity phosphatase; can dephosphorylate both phosphotyrosine and phosphoserine or phosphothreonine residues (PubMed:24714587, PubMed:38225265). Activates the JNK signaling pathway (PubMed:11717427). Inhibits T-cell receptor signaling and T-cell mediated immune responses, acting, at least in part, by inducing degradation of E3 ubiquitin ligase UBR2 (PubMed:24714587, PubMed:38225265). Dephosphorylates and thereby induces 'Lys-48'-linked ubiquitination of UBR2, leading to proteasomal degradation of UBR2 (PubMed:38225265). Dephosphorylates and thereby inactivates tyrosine kinase LCK (PubMed:24714587). Inhibits UBR2-mediated 'Lys-63'-linked ubiquitination of LCK (PubMed:38225265). May play a role in B-cell receptor (BCR) signaling and B-cell function (By similarity).

Drugs associated with DUSP22

BML-260

Target

DUSP22 x UCP1

Mechanism

DUSP22 inhibitors [+1]

Active Org.

Shanghai Institutes for Biological Sciences CAS

Originator Org.

Shanghai Institutes for Biological Sciences CAS

Active Indication

Obesity

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with DUSP22

100 Translational Medicine associated with DUSP22

0 Patents (Medical) associated with DUSP22

203

Literatures (Medical) associated with DUSP22

01 Feb 2025·Human Pathology

Systemic ALK-negative anaplastic large cell lymphoma: Insights into morphologic, immunophenotypic, genetic and molecular characteristics

Review

Author: Medeiros, L Jeffrey ; Xu, Jie ; Fan, Guang ; Li, Shaoying ; Medeiros, L. Jeffrey ; Xie, Wei

Anaplastic large cell lymphoma (ALCL) is a mature T-cell neoplasm characterized by large pleomorphic cells, often with horseshoe- or kidney-shaped nuclei and abundant cytoplasm (hallmark cells), and uniformly strong CD30 expression. Based on ALK expression or ALK rearrangement, ALCL is further classified into ALK-positive (ALK+) and ALK-negative types. This review focuses on the clinicopathologic, immunophenotypic, cytogenetic and molecular features of systemic ALK-negative ALCL. These patients are usually older adults who present with advanced stage disease and often a poor prognosis. ALK-negative ALCL is morphologically indistinguishable from the common pattern of ALK+ ALCL, but some cases show non-common morphology, such as "donut cells", Hodgkin-like features. ALK-negative ALCL is often negative for T-cell antigens (so-called "antigen loss") and in some cases can have a "null" immunophenotype and be confused with other hematopoietic and non-hematopoietic neoplasms. Recurrent genetic/molecular alterations have been identified in systemic ALK-negative ALCL, including rearrangements of DUSP22, TP63, JAK2, FRK, MYC, ROS1 and TYK2; mutations of JAK1, STAT3 and MSCE; and aberrant expression of ERBB4. Some of these alterations may have prognostic significance and/or provide potential therapeutic targets. Data support the idea that ALK-negative ALCL with DUSP22 rearrangement is a distinctive variant due to its unique morphologic, immunophenotypic and molecular features. Gene expression profiling data have shown that ALK-negative ALCL has distinctive molecular signatures, different from ALK+ ALCL and other T-cell lymphomas. Better understanding of the morphologic, immunophenotypic, genetic and molecular features of ALK-negative ALCL will help establish the correct diagnosis, guide therapeutic strategies and improve patient outcomes.

01 Dec 2024·Journal of Hematopathology

Systemic ALK-negative anaplastic large cell lymphoma with NPM1::TYK2 rearrangement

Article

Author: Johnson, Mckinzie ; Willard, Nicholas ; Pan, Zenggang

Anaplastic large cell lymphoma (ALCL) is a rare subtype of non-Hodgkin lymphoma, with most cases harboring ALK gene rearrangement (ALK + ALCL); however, 20-50% of ALCLs do not have the rearrangement (ALK- ALCL) but exhibit distinct genetic alterations. In this report, we present an unusual case of systemic ALK- ALCL with NPM1::TYK2 fusion. Diagnosis of this case was challenging prior to the NGS findings. A comprehensive panel of immunohistochemical and in-situ hybridization studies was conducted. FISH assays were utilized to target the rearrangements of DUSP22 and TP63 genes. Moreover, next-generation sequencing (NGS) assays were performed to detect clonal rearrangements of IGH and TRG genes, somatic mutations, and potential fusions. The lymphoma cells in this case are negative for all hematolymphoid markers stained, except for CD30 expression and focal and weak CD43 expression. However, NGS studies detected clonal TRG rearrangement and NPM1::TYK2 rearrangement, which aid in the diagnosis of ALK- ALCL. NPM1::TYK2 rearrangement is a rare genetic alteration that has been reported in rare cases of primary cutaneous ALCL, mycosis fungoides, and lymphomatoid papulosis. To the best of our knowledge, this is the first reported instance of such rearrangement in systemic ALK- ALCL.

01 Oct 2024·Journal of Atherosclerosis and Thrombosis

JNK Pathway-Associated Phosphatase Deficiency Facilitates Atherosclerotic Progression by Inducing T-Helper 1 and 17 Polarization and Inflammation in an ERK- and NF-κB Pathway-Dependent Manner

Article

Author: Fang, Mingcheng ; Hong, Jingxuan ; Guo, Yansong ; Chen, Xinjing

AIMJNK pathway-associated phosphatase (JKAP) regulates T cell-mediated immunity and inflammation, which are involved in atherosclerosis pathogenesis. This study investigated the effects of JKAP on T-helper (Th) cell polarization, inflammation, and atherosclerotic progression.METHODSSerum JKAP levels were measured in 30 patients with coronary heart disease (CHD) and 30 controls. CHD blood naïve CD4^＋ T cells were acquired, followed by JKAP overexpression and knockdown with or without treatment with PD98059 (ERK inhibitor) or BAY-11-7082 (NF-κB inhibitor) in vitro. CD4^＋ T-cell conditional JKAP ablation mice were established in vivo, followed by the construction of an atherosclerosis model.RESULTSJKAP was reduced and negatively correlated with the Gensini score, CRP, Th1 cells, Th17 cells, and proinflammatory cytokines in patients with CHD. In vitro, JKAP overexpression suppressed Th1 and Th17 cell differentiation and proinflammatory cytokines, whereas JKAP knockdown exerted the opposite effect; however, JKAP modification did not affect Th2 cell differentiation. Interestingly, JKAP negatively regulated the ERK and NF-κB pathways; meanwhile, the PD98059 and BAY-11-7082 treatments repressed Th1 and Th17 cell differentiation, and attenuated the effect of JKAP knockdown on these indices. In vivo, conditional CD4^＋ T-cell JKAP ablation increased Th1 and Th17 cell polarization in the spleen, lymph node, blood, and/or aortic root. Furthermore, CD4^＋ T-cell conditional JKAP ablation exaggerated atherosclerotic lesions in the aorta, elevated CD4⁺ cell infiltration and proinflammatory cytokines in the aortic root, and activated the ERK and NF-κB pathways in the aortic root.CONCLUSIONJKAP ablation facilitates atherosclerosis progression by promoting Th1 and 17 polarization and inflammation through regulation of the ERK and NF-κB pathways.

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DUSP22

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