LRCH4

Last update 08 May 2025

Basic Info

Synonyms

leucine rich repeats and calponin homology domain containing 4, Leucine-rich neuronal protein, Leucine-rich repeat and calponin homology domain-containing protein 4

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Introduction

Accessory protein that regulates signaling by multiple TLRs, acting as a broad-spanning regulator of the innate immune response. In macrophages, binds LPS and promotes proper docking of LPS in lipid raft membrane. May be required for lipid raft maintenance.

100 Clinical Results associated with LRCH4

100 Translational Medicine associated with LRCH4

0 Patents (Medical) associated with LRCH4

Literatures (Medical) associated with LRCH4

01 Aug 2024·Combinatorial Chemistry & High Throughput Screening

Knockdown of LRCH4 Remodels Tumor Microenvironment Through Inhibiting YAP and TGF-β/Smad Signaling Pathway in Colorectal Cancer

Article

Author: Li, Zhiwen ; Wang, Xianren ; Cui, Zhenhua ; Lv, Yanfeng

Background::Colorectal cancer is one of the most common gastrointestinal malignancies worldwide. LRCH4 is the top 1 gene associated with an unfavorable prognosis in colorectal cancer.Methods::Here, we reported that the knockdown of LRCH4 inhibited the proliferation, migration and invasion in HT29 cells.Results::The activity of Yes-Associated Protein (YAP), a transcription factor in the Hppo-YAP signaling pathway, was significantly inhibited by LRCH4-siRNA. LRCH4 knockdown also reversed the EMT and regulated the expression of extracellular matrix (ECM) protein, Fibronectin and Collagen IV in HT29 cells. In addition, the TGF-β/Smad signaling pathway, as the downstream pathway of Yap, was also inhibited by LRCH4 knockdown.Conclusion::Knockdown of LRCH4 involved in the regulation of ECM and EMT and inhibited YAP and the TGF-β/Smad signaling pathway in colorectal cancer cells. Our study provided a mechanism of LRCH4 on colorectal cancer cells, and a new potential target for clinical tumor treatment

01 Mar 2021·Clinical and Translational OncologyQ3 · MEDICINE

Identifying a novel 5-gene signature predicting clinical outcomes in acute myeloid leukemia

Q3 · MEDICINE

Article

Author: Shi, X ; Sha, K ; Zhang, P ; Lu, Y ; Pei, R ; Fan, Z ; Chen, L

BACKGROUNDAcute myeloid leukemia (AML) is the most common type of acute leukemia and biologically heterogeneous diseases with poor prognosis. Thus, we aimed to identify prognostic markers to effectively predict the prognosis of AML patients and eventually guide treatment.METHODSPrognosis-associated genes were determined by Kaplan-Meier and multivariate analyses using the expression and clinical data of 173 AML patients from The Cancer Genome Atlas database and validated in an independent Oregon Health and Science University dataset. A prognostic risk score was computed based on a linear combination of 5-gene expression levels using the regression coefficients derived from the multivariate logistic regression model. The classification of AML was established by unsupervised hierarchical clustering of CALCRL, DOCK1, PLA2G4A, FCHO2 and LRCH4 expression levels.RESULTSHigh FCHO2 and LRCH4 expression was related to decreased mortality. While high CALCRL, DOCK1, PLA2G4A expression was associated with increased mortality. The risk score was predictive of increased mortality rate in AML patients. Hierarchical clustering analysis of the five genes discovered three clusters of AML patients. The cluster1 AML patients were associated with lower cytogenetics risk than cluster2 or 3 patients, and better prognosis than cluster3 patients (P values < 0.05 for all cases, fisher exact test or log-rank test).CONCLUSIONThe gene panel comprising CALCRL, DOCK1, PLA2G4A, FCHO2 and LRCH4 as well as the risk score may offer novel prognostic biomarkers and classification of AML patients to significantly improve outcome prediction.

01 Feb 2019·Journal of Biological ChemistryQ2 · BIOLOGY

Leucine-rich repeats and calponin homology containing 4 (Lrch4) regulates the innate immune response

Q2 · BIOLOGY

Article

Author: Gruzdev, Artiom ; Fessler, Michael B ; Draper, David W ; Henderson, Michael W ; Lin, Wan-Chi ; Gowdy, Kymberly M ; Guardiola, John J ; Azzam, Kathleen M ; Merrick, B Alex ; Mueller, Geoffrey A ; Gabor, Kristin A ; Lowe, Julie M ; Madenspacher, Jennifer H ; Aloor, Jim J

Toll-like receptors (TLRs) are pathogen-recognition receptors that trigger the innate immune response. Recent reports have identified accessory proteins that provide essential support to TLR function through ligand delivery and receptor trafficking. Herein, we introduce leucine-rich repeats (LRRs) and calponin homology containing 4 (Lrch4) as a novel TLR accessory protein. Lrch4 is a membrane protein with nine LRRs in its predicted ectodomain. It is widely expressed across murine tissues and has two expression variants that are both regulated by lipopolysaccharide (LPS). Predictive modeling indicates that Lrch4 LRRs conform to the horseshoe-shaped structure typical of LRRs in pathogen-recognition receptors and that the best structural match in the protein database is to the variable lymphocyte receptor of the jawless vertebrate hagfish. Silencing Lrch4 attenuates cytokine induction by LPS and multiple other TLR ligands and dampens the in vivo innate immune response. Lrch4 promotes proper docking of LPS in lipid raft membrane microdomains. We provide evidence that this is through regulation of lipid rafts as Lrch4 silencing reduces cell surface gangliosides, a metric of raft abundance, as well as expression and surface display of CD14, a raft-resident LPS co-receptor. Taken together, we identify Lrch4 as a broad-spanning regulator of the innate immune response and a potential molecular target in inflammatory disease.

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LRCH4

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