Last update 01 Nov 2024

SSH2

Last update 01 Nov 2024

Basic Info

Synonyms

hSSH-2L, KIAA1725, Protein phosphatase Slingshot homolog 2

+ [5]

Introduction

Protein phosphatase which regulates actin filament dynamics. Dephosphorylates and activates the actin binding/depolymerizing factor cofilin, which subsequently binds to actin filaments and stimulates their disassembly. Inhibitory phosphorylation of cofilin is mediated by LIMK1, which may also be dephosphorylated and inactivated by this protein.

Drugs associated with SSH2

CN115991789

Patent Mining

Target

BCR x SSH2

Mechanism-

Active Org.

Huazhong University of Science & Technology

Originator Org.

Huazhong University of Science & Technology

Active Indication

Hemic and Lymphatic Diseases

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with SSH2

100 Translational Medicine associated with SSH2

0 Patents (Medical) associated with SSH2

Literatures (Medical) associated with SSH2

19 Aug 2023·Cardiovascular Research

Lipocalin 10 is essential for protection against inflammation-triggered vascular leakage by activating LDL receptor-related protein 2-slingshot homologue 1 signalling pathway

Article

Author: Zhao, Hongyan ; Peng, Tianqing ; Du, Wa ; Chen, Jing ; Fan, Guo-Chang ; Gao, Chen ; Wang, Chunting ; Liu, Yueying ; Wang, Yigang ; Ma, Chengen ; Cui, Shu-Nan ; Fan, Yanbo ; Sadayappan, Sakthivel ; Yang, Hui-Hui ; Wang, Peng ; Wang, Xiaohong ; Huang, Wei

AbstractAimsSystemic inflammation occurs commonly during many human disease settings and increases vascular permeability, leading to organ failure, and lethal outcomes. Lipocalin 10 (Lcn10), a poorly characterized member of the lipocalin family, is remarkably altered in the cardiovascular system of human patients with inflammatory conditions. Nonetheless, whether Lcn10 regulates inflammation-induced endothelial permeability remains unknown.Methods and resultsSystemic inflammation models were induced using mice by injection of endotoxin lipopolysaccharide (LPS) or caecal ligation and puncture (CLP) surgery. We observed that the expression of Lcn10 was dynamically altered only in endothelial cells (ECs), but not in either fibroblasts or cardiomyocytes isolated from mouse hearts following the LPS challenge or CLP surgery. Using in vitro gain- and loss-of-function approaches and an in vivo global knockout mouse model, we discovered that Lcn10 negatively regulated endothelial permeability upon inflammatory stimuli. Loss of Lcn10 augmented vascular leakage, leading to severe organ damage and higher mortality following LPS challenge, compared to wild-type controls. By contrast, overexpression of Lcn10 in ECs displayed opposite effects. A mechanistic analysis revealed that both endogenous and exogenous elevation of Lcn10 in ECs could activate slingshot homologue 1 (Ssh1)-Cofilin signalling cascade, a key axis known to control actin filament dynamics. Accordingly, a reduced formation of stress fibre and increased generation of cortical actin band were exhibited in Lcn10-ECs, when compared to controls upon endotoxin insults. Furthermore, we identified that Lcn10 interacted with LDL receptor-related protein 2 (LRP2) in ECs, which acted as an upstream factor of the Ssh1-Confilin signalling. Finally, injection of recombinant Lcn10 protein into endotoxic mice showed therapeutic effects against inflammation-induced vascular leakage.ConclusionThis study identifies Lcn10 as a novel regulator of EC function and illustrates a new link in the Lcn10-LRP2-Ssh1 axis to controlling endothelial barrier integrity. Our findings may provide novel strategies for the treatment of inflammation-related diseases.

01 Jun 2023·Neuroscience bulletin

TRPM7 Kinase Domain is Part of the Rac1-SSH2-cofilin Complex Regulating F-actin in the Mouse Nervous System.

Letter

Author: Chen, Cui ; Li, Wei ; Chang, Junzhuang ; Abumaria, Nashat

01 Jan 2023·Pharmacogenomics and personalized medicine

Genome-Wide Identification of lncRNA and mRNA for Diagnosing Type 2 Diabetes in Saudi Arabia.

Article

Author: Albogami, Sarah

PurposeAccording to the World Health Organization, Saudi Arabia ranks seventh worldwide in the number of patients with diabetes mellitus. To our knowledge, no research has addressed the potential of noncoding RNA as a diagnostic and/or management biomarker for patients with type 2 diabetes mellitus (T2DM) living in high-altitude areas. This study aimed to identify molecular biomarkers influencing patients with T2DM living in high-altitude areas by analyzing lncRNA and mRNA.Patients and MethodsRNA sequencing and bioinformatics analyses were used to identify significantly expressed lncRNAs and mRNAs in T2DM and healthy control groups. Coding potential was analyzed using coding-noncoding indices, the coding potential calculator, and PFAM, and the lncRNA function was predicted using Pearson's correlation. Differentially expressed transcripts between the groups were identified, and Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed to identify the biological functions of both lncRNAs and mRNAs.ResultsWe assembled 1766 lncRNAs in the T2DM group, of which 582 were novel. This study identified three lncRNA target genes (KLF2, CREBBP, and REL) and seven mRNAs (PIK3CD, PIK3R5, IL6R, TYK2, ZAP70, LAMTOR4, and SSH2) significantly enriched in important pathways, playing a role in the progression of T2DM.ConclusionTo the best of our knowledge, this comprehensive study is the first to explore the applicability of certain lncRNAs as diagnostic or management biomarkers for T2DM in females in Taif City, Saudi Arabia through the genome-wide identification of lncRNA and mRNA profiling using RNA seq and bioinformatics analysis. Our findings could help in the early diagnosis of T2DM and in designing effective therapeutic targets.

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SSH2

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