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Last update 08 May 2025

GPR161

Last update 08 May 2025

Basic Info

Synonyms

G protein-coupled receptor 161, G-protein coupled receptor 161, G-protein coupled receptor RE2

+ [2]

Introduction

Key negative regulator of Shh signaling, which promotes the processing of GLI3 into GLI3R during neural tube development. Recruited by TULP3 and the IFT-A complex to primary cilia and acts as a regulator of the PKA-dependent basal repression machinery in Shh signaling by increasing cAMP levels, leading to promote the PKA-dependent processing of GLI3 into GLI3R and repress the Shh signaling. In presence of SHH, it is removed from primary cilia and is internalized into recycling endosomes, preventing its activity and allowing activation of the Shh signaling. Its ligand is unknown (By similarity).

Drugs associated with GPR161

CN117567642

Patent Mining

Target

GPR161

Mechanism-

Active Org.

Shanghai Shen Lian Biomedical Corp.

Originator Org.

Shanghai Shen Lian Biomedical Corp.

Active Indication

Virus Diseases

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Targeting GPR161 (Omeros)

Target

GPR161

Mechanism

GPR161 antagonists

Active Org.-

Originator Org.

Omeros Corp.

Active Indication-

Inactive Indication

Brain Injuries [+2]

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with GPR161

100 Translational Medicine associated with GPR161

0 Patents (Medical) associated with GPR161

127

Literatures (Medical) associated with GPR161

01 Dec 2024·Translational Cancer Research

Genomic landscape of medulloblastoma subtypes in an Asian cohort

Article

Author: Han, Dongming ; Li, Jiankang ; Jin, Xin

BackgroundMedulloblastoma (MB) is a highly malignant childhood brain tumor. Previous research on the genetic underpinnings of MB subtypes has predominantly focused on European and American cohorts. Given the notable genetic differences between Asian and other populations, a subtype-specific study on an Asian cohort is essential to provide comprehensive insights into MB within this demographic. The aim of this study is to investigate the genomic landscape of MB subtypes in an Asian cohort to better understand the genetic variations and potential implications for clinical practice.MethodsWe conducted a study on an Asian cohort comprising 113 MB patients. Genomic sequencing was performed using MGISEQ-2000 platform. We analyzed the participants' characteristics and compared them with previous studies. All germline variants of the ten susceptibility genes of interest (APC, BRCA2, PTCH1, PTCH2, ELP1, SUFU, CTNNB1, SMARCA4, GPR161, and TP53) were annotated and validated.ResultsOur study identified 14 valid germline variants that met our criteria, with these variants being detected in the genes APC, BRCA2, PTCH1, PTCH2, ELP1, and SUFU. Of these, six variants were classified as pathogenic in ClinVar: two in PTCH2 (c.C1573T), one in ELP1 (c.C583T), and three in PTCH1 (c.G1370T, c.C2066T, c.C529T). The remaining eight variants were of uncertain significance, including those in SUFU (c.T833C), ELP1 (c.T2A), BRCA2 (c.G7488C), and APC (c.C3247A, c.A1G, c.A8042G, c.A3056G, c.G822C). Our findings highlight a subtype-based germline variant landscape specific to the Asian cohort and reinforce the connection between SUFU, PTCH1, and the SHH subtype of MB. Additionally, the identification of ELP1-related cases supports the newest findings in this area and provides typical copy number variation (CNV) results for future investigation.ConclusionsThis study provides valuable insights into the genetic landscape of MB in an Asian cohort, emphasizing the importance of population-specific research. The subtype-specific germline variant landscape identified in this study contributes to the understanding of MB and its genetic underpinnings in Asian populations, potentially guiding future research and therapeutic strategies.

01 Dec 2024·Veterinary Microbiology

Dihydrolipoamide acetyltransferase is a key factor mediating adhesion and invasion of host cells by Mycoplasma synoviae

Article

Author: Xing, Xiaoyong ; Wu, Xiaochun ; Zhao, Yunhai ; Zhang, Yuting ; Wang, Qing ; Bao, Shijun ; Quan, Guomei ; He, Xiaoxiao ; Ma, Haiyun

Mycoplasma synoviae is a significant avian pathogen responsible for chronic respiratory diseases, arthritis, and infectious synovitis in chickens and turkeys. These infections result in substantial economic losses to the global poultry industry. Dihydrolipoamide acetyltransferase (E2) is a multifunctional protein that plays an indispensable role in energy metabolism and redox balance and is also a key virulence factor of various pathogens. In this study, we used the avian pathogen M. synoviae as a model to identify the role of the E2 protein in the colonization and invasion of host cells. First, we prepared the polyclonal antibody of recombinant E2 (rE2) protein and found that the rE2 antibody had a strong complement-activating ability. E2 was found to be distributed in the cytoplasm and cell membrane of M. synoviae by immunoelectron microscopy. E2 localized on the cell membrane is a key factor in the adhesion of M. synoviae and has good immunogenicity. Enzyme-linked immunosorbent assay showed that the binding of rE2 to membrane proteins of chicken embryo fibroblasts (DF-1) was dose-dependent, and antiserum effectively inhibited this binding ability. Furthermore, E2 interacted with various components of the host extracellular matrix (ECM) and promoted the conversion of plasminogen to plasmin through terephthalic acid (tPA). In addition, E2 can enhance the ability of M. synoviae to invade DF-1 cells, which was significantly reduced after treatment with anti-E2 serum. These results indicate that E2 is an adhesion- and invasion-related protein and may be involved in the pathogenesis of M. synoviae, which provides new ideas for studying the pathogenesis of M. synoviae and preparing subunit vaccines.

01 Dec 2024·Microbiological Research

Sterol regulatory element-binding proteins mediate intrinsic fungicide tolerance and antagonism in the fungal biocontrol agent Clonostachys rosea IK726

Article

Author: Dubey, Mukesh ; Ruus, Alma Gustavsson ; Rafiei, Vahideh ; Karlsson, Magnus ; Piombo, Edoardo ; Jensen, Dan Funck ; Tzelepis, Georgios

Sterol regulatory element-binding proteins (SREBPs) are transcription factors governing various biological processes in fungi, including virulence and fungicide tolerance, by regulating ergosterol biosynthesis and homeostasis. While studied in model fungal species, their role in fungal species used for biocontrol remains elusive. This study delves into the biological and regulatory function of SREBPs in the fungal biocontrol agent (BCA) Clonostachys rosea IK726, with a specific focus on fungicide tolerance and antagonism. Clonostachys rosea genome contains two SREBP coding genes (sre1 and sre2) with distinct characteristics. Deletion of sre1 resulted in mutant strains with pleiotropic phenotypes, including reduced C. rosea growth on medium supplemented with prothioconazole and boscalid fungicides, hypoxia mimicking agent CoCl₂ and cell wall stressor SDS, and altered antagonistic abilities against Botrytis cinerea and Rhizoctonia solani. However, Δsre2 strains showed no significant effect. Consistent with the gene deletion results, overexpression of sre1 in Saccharomyces cerevisiae enhanced tolerance to prothioconazole. The functional differentiation between SRE1 and SRE2 was elucidated by the yeast-two-hybridization assay, which showed an interaction between SREBP cleavage-activating protein (SCAP) and SRE1 but not between SRE2 and SCAP. Transcriptome analysis of the Δsre1 strain unveiled SRE1-mediated expression regulation of genes involved in lipid metabolism, respiration, and xenobiotic tolerance. Notably, genes coding for antimicrobial compounds chitinases and polyketide synthases were downregulated, aligning with the altered antagonism phenotype. This study uncovers the role of SREBPs in fungal BCAs, providing insights for C. rosea IK726 application into integrated pest management strategies.

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GPR161

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