LRCH1

Last update 08 May 2025

Basic Info

Synonyms

Calponin homology domain-containing protein 1, CHDC1, KIAA1016

+ [5]

Introduction

Acts as a negative regulator of GTPase CDC42 by sequestering CDC42-guanine exchange factor DOCK8. Probably by preventing CDC42 activation, negatively regulates CD4(+) T-cell migration.

100 Clinical Results associated with LRCH1

100 Translational Medicine associated with LRCH1

0 Patents (Medical) associated with LRCH1

Literatures (Medical) associated with LRCH1

01 Dec 2024·Alzheimer's & Dementia

Whole‐Genome Sequencing Study in Koreans Identifies Novel Loci for Alzheimer Disease

Article

Author: Jun, Gyungah R ; Won, Sungho ; Kang, Moonil ; Lee, Kun Ho ; Zhu, Congcong ; Kang, Sarang ; Park, Hyeonseul ; Seo, Eun Hyun ; Choi, Kyu Yeong ; Farrer, Lindsay A ; Gim, Jungsoo ; Farrell, John J

AbstractBackgroundWith a rapidly aging population, South Korea anticipates a surge in Alzheimer disease (AD). However, the genetic basis of AD in Koreans is not well understood.MethodWe sequenced the genomes of 3,540 Koreans (1,583 AD cases and 1,957 controls) older than age 60 and performed a genome‐wide association study (GWAS) of AD using logistic regression models that included covariates for age, sex, five ancestry principal components, and an empirical genetic relationship matrix. We also conducted association tests in subgroups stratified by APOE ε4 status or sex. Findings from the Korean sample were combined with results from two Japanese GWAS datasets using the inverse‐variance meta‐analysis method. We also performed gene‐based tests of aggregated rare variants in the Korean dataset. Novel findings were evaluated by pathway enrichment analysis and by differential gene expression analysis in brain tissue from controls and AD cases who were either cognitively impaired or healthy prior to death.ResultWe identified genome‐wide significant (GWS) associations (P < 5.0 × 10‐8) with two well‐established AD loci (APOE and SORL1) in the total sample and with one novel locus, ROCK2 (rs76484417, P = 2.71 × 10‐8) among APOE ε4 non‐carriers. Another novel study‐wide significant association (P < 2.47 × 10‐6) was found with aggregated rare variants in MICALL1 (P = 9.04 × 10‐7). We also observed suggestive associations (P < 1.0 × 10‐6) with 14 novel loci (MSX1, BCL11A, ARMH3, CTNNA3, YTHDF1P1, GRM3, LINC02479, LRCH1, COL9A1, TTC8, MCTP2, DLGAP2, TBC1D32, and EXD2). Expression of several novel genes, including ROCK2 and MICALL1, was significantly different in multiple cortical regions in AD cases compared to controls (P < 3.33 × 10‐3). ROCK2 was also differentially expressed between AD cases with and without cognitive impairment (P = 1.34 × 10‐4).ConclusionWe identified GWS and suggestive association for AD with several loci in Koreans and Japanese not previously observed in other populations. Our results provide additional insight into genetic mechanisms leading to AD and cognitive resilience, as well as emphasize the need for further genetic studies of East Asian populations.

01 Apr 2024·Development

The Shot CH1 domain recognises a distinct form of F-actin during Drosophila oocyte determination.

Article

Author: Squires, Iolo ; Nashchekin, Dmitry ; Prokop, Andreas ; St Johnston, Daniel

In Drosophila, only one cell in a multicellular female germline cyst is specified as an oocyte and a similar process occurs in mammals. The symmetry-breaking cue for oocyte selection is provided by the fusome, a tubular structure connecting all cells in the cyst. The Drosophila spectraplakin Shot localises to the fusome and translates its asymmetry into a polarised microtubule network that is essential for oocyte specification, but how Shot recognises the fusome is unclear. Here, we demonstrate that the actin-binding domain (ABD) of Shot is necessary and sufficient to localise Shot to the fusome and mediates Shot function in oocyte specification together with the microtubule-binding domains. The calponin homology domain 1 of the Shot ABD recognises fusomal F-actin and requires calponin homology domain 2 to distinguish it from other forms of F-actin in the cyst. By contrast, the ABDs of utrophin, Fimbrin, Filamin, Lifeact and F-tractin do not recognise fusomal F-actin. We therefore propose that Shot propagates fusome asymmetry by recognising a specific conformational state of F-actin on the fusome.

24 Aug 2023·British Journal of Cancer

Probing the diabetes and colorectal cancer relationship using gene – environment interaction analyses

Article

Author: Larsson, Susanna C ; Diez-Obrero, Virginia ; Li, Li ; Moreno, Victor ; Woods, Michael O ; Lin, Yi ; Carreras-Torres, Robert ; Newton, Christina C ; Figueiredo, Jane C ; Jordahl, Kristina ; Tsilidis, Kostas K ; Jenkins, Mark A ; Obon-Santacana, Mireia ; van Duijnhoven, Franzel J B ; Su, Yu-Ru ; Dimou, Niki ; Brenner, Hermann ; Gauderman, W James ; Conti, David V ; Stern, Mariana C ; Keku, Temitope O ; Rennert, Gad ; Kundaje, Anshul ; Pharoah, Paul D P ; Papadimitriou, Nikos ; Bézieau, Stéphane ; Baurley, James W ; Mahesworo, Bharuno ; Cenggoro, Tjeng Wawan ; Peoples, Anita R ; Aglago, Elom K ; Palmer, Julie R ; Kawaguchi, Eric ; Qu, Conghui ; Kim, Andre E ; Shcherbina, Anna ; Vodickova, Ludmila ; Dampier, Christopher H ; Harrison, Tabitha A ; Bishop, D Timothy ; Gsur, Andrea ; Ulrich, Cornelia M ; Budiarto, Arif ; Platz, Elizabeth A ; Hoffmeister, Michael ; Casey, Graham ; Giles, Graham G ; Campbell, Peter T ; Thomas, Duncan C ; Chang-Claude, Jenny ; Chanock, Stephen J ; Gunter, Marc J ; Arndt, Volker ; White, Emily ; Bouras, Emmanouil ; Um, Caroline Y ; Ose, Jennifer ; Potter, John D ; Barry, Elizabeth L ; Chan, Andrew T ; Wolk, Alicja ; Bien, Stephanie A ; Thibodeau, Stephen N ; Pardamean, Bens ; Tian, Yu ; Tangen, Catherine M ; Vodicka, Pavel ; Newcomb, Polly A ; Drew, David A ; Le Marchand, Loic ; Devall, Matthew ; Schoen, Robert E ; Visvanathan, Kala ; Chen, Xuechen ; Hsu, Li ; Berndt, Sonja I ; Scacheri, Peter C ; Flanagan, Orlagh ; Huyghe, Jeroen R ; Peters, Ulrike ; Pai, Rish K ; Hidaka, Akihisa ; Morrison, John ; Lewinger, Juan Pablo ; Gallinger, Steven ; Murphy, Neil ; Ruiz-Narvaez, Edward ; Gruber, Stephen B

AbstractBackgroundDiabetes is an established risk factor for colorectal cancer. However, the mechanisms underlying this relationship still require investigation and it is not known if the association is modified by genetic variants. To address these questions, we undertook a genome-wide gene-environment interaction analysis.MethodsWe used data from 3 genetic consortia (CCFR, CORECT, GECCO; 31,318 colorectal cancer cases/41,499 controls) and undertook genome-wide gene-environment interaction analyses with colorectal cancer risk, including interaction tests of genetics(G)xdiabetes (1-degree of freedom; d.f.) and joint testing of Gxdiabetes, G-colorectal cancer association (2-d.f. joint test) and G-diabetes correlation (3-d.f. joint test).ResultsBased on the joint tests, we found that the association of diabetes with colorectal cancer risk is modified by loci on chromosomes 8q24.11 (rs3802177,SLC30A8 –ORAA: 1.62, 95% CI: 1.34–1.96; ORAG: 1.41, 95% CI: 1.30–1.54; ORGG: 1.22, 95% CI: 1.13–1.31;p-value3-d.f.: 5.46 × 10−11) and 13q14.13 (rs9526201,LRCH1 –ORGG: 2.11, 95% CI: 1.56–2.83; ORGA: 1.52, 95% CI: 1.38–1.68; ORAA: 1.13, 95% CI: 1.06–1.21;p-value2-d.f.: 7.84 × 10−09).DiscussionThese results suggest that variation in genes related to insulin signaling (SLC30A8) and immune function (LRCH1) may modify the association of diabetes with colorectal cancer risk and provide novel insights into the biology underlying the diabetes and colorectal cancer relationship.

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LRCH1

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