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Last update 08 May 2025

MSRB3

Last update 08 May 2025

Basic Info

Synonyms

DFNB74, DKFZp686C1178, FLJ36866

+ [3]

Introduction

Catalyzes the reduction of free and protein-bound methionine sulfoxide to methionine. Isoform 2 is essential for hearing.

Drugs associated with MSRB3

Naphthoquinone derivatives 11

Target

MSRA x MSRB1 x MSRB2 x MSRB3

Mechanism

MSRA modulators [+3]

Active Org.

North South University

Originator Org.-

Active Indication

MRSA - Methicillin resistant Staphylococcus aureus infection [+1]

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with MSRB3

100 Translational Medicine associated with MSRB3

0 Patents (Medical) associated with MSRB3

107

Literatures (Medical) associated with MSRB3

01 Feb 2025·Animal Genetics

Comprehensive genomic analysis and selection signature detection in endangered Beigang pigs using whole‐genome sequencing data

Article

Author: Gao, Hui ; Zhang, Xiaowei ; Ma, Xuejian ; Han, He ; Zhang, Zhenyang ; Liu, Shengqiang ; Pan, Yuchun ; Wang, Meng ; Shi, Jinhu ; Chen, Zitao ; Gu, Jiamin ; Wang, Qishan

AbstractThe Beigang pig was recently identified as one of the endangered breeds during a Chinese indigenous pig genetic resource survey. The Beigang breed is notable for its remarkable roughage tolerance and high reproductive capacity according to historical records. Morphologically, the Beigang pig resembles many indigenous pigs in eastern China, especially in its large ears. This makes the Beigang pig a valuable reference for studying the genetic mechanisms on large ear size in pigs. However, there is currently a lack of clear understanding regarding the genetic structure and inbreeding levels of the Beigang pig population. This study used whole‐genome sequencing data from Beigang pig (N = 145 pigs) and integrated genetic information from commercial pigs and indigenous pigs in eastern China to conduct a comprehensive analysis of the Beigang pig's genetic structure. Three selection signal detection methods—runs of homozygosity, fixation index, and integrated haplotype score—were employed to explore the differences in genomic selection signatures between Beigang pig and other pig populations. Additionally, we used a public project for regulatory variants discovery and molecular phenotype prediction in farm animal species called FarmGtex to explore the expression of three genes (WIF1, LEMD3, and MSRB3) related to ear size in Beigang pig. This research identified five homozygous variant sites in the WIF1 gene as important candidate loci potentially influencing ear size in Beigang pig. The results indicate that the Beigang pig holds a unique status among Chinese indigenous pigs, characterized by high genetic diversity and low levels of inbreeding. The study also revealed that WIF1 may play a significant role in influencing ear size in this breed. These findings contribute to a deeper understanding of the population structure and genetic characteristics of Beigang pig.

01 Oct 2024·Human Pathology

Beneath HMGA2 alterations in pleomorphic adenomas: Pathological, immunohistochemical, and molecular insights

Article

Author: Houessinon, A. ; Jankowski, R. ; Calugaru, V. ; Villepelet, A. ; Gilain, L. ; Bach, C. ; Salas, S. ; Laé, Marick ; Delord, J.P. ; Lesnik, M. ; Bertolus, C. ; Rolland, F. ; Queiros, C. ; Sterkers, O. ; Righini, C.A. ; Garrel, R. ; Michel, J. ; Varoquaux, A. ; Wassef, M. ; Rambeau, A. ; Cristofari, J.P. ; Pestre, J. ; Céruse, Philippe ; Obongo-Anga, F.R. ; Coste, A. ; Malard, O. ; Dolivet, G. ; Philouze, Pierre ; Nguyen, F. ; Lelonge, Y. ; Coutte, A. ; Huguet, F. ; Calais, G. ; Benzerdjeb, N. ; Renard, S. ; Ferrand, F.R. ; Hans, S. ; de Gabory, L. ; Benzerdjeb, Nazim ; Boulagnon-Rombi, C. ; Lamuraglia, M. ; Delgrande, J. ; Poissonnet, G. ; Doré, M. ; Laadhari, M. ; Baglin, A.C. ; Bernadach, M. ; Cupissol, D. ; Garcier, M. ; Valette, G. ; Wong, S. ; Schultz, P. ; Clatot, F. ; Baglin, Anne-Catherine ; Testelin, S. ; Wagner, I. ; Strunski, V. ; Kaci, R. ; Fakhry, N. ; Even, C. ; Philouze, P. ; Bastit, V. ; Toussaint, B. ; Frandon, J. ; Mirafzal, S. ; Marchand, C. ; Wassef, Michel ; Onea, M. ; Kreps, S. ; Eker, E. ; Constans, J.M. ; Castain, C. ; de Kermadec, H. ; Le Tourneau, C. ; Benezery, K. ; Brugel, L. ; Mihaela, Onea ; Hourseau, M. ; Timochenko, A. ; Musat, E. ; Marie, J.-P. ; Lagrange, A. ; Lépine, Charles ; Gauthier, H. ; Sacino, F. ; Lefebvre, G. ; Lae, M. ; Halimi, C. ; Grayeli, A.Bozorg ; Ala-Eddine, C. ; Lang, P. ; Pons, C. ; Lallemant, B. ; Jadaud, E. ; Devauchelle, B. ; Noel, G. ; Pouliquen, C. ; Lagarde, F. ; Sudaka, Anne ; Guihard, S. ; Laccoureye, L. ; Biet, A. ; Simonaggio, A. ; Boisselier, P. ; Cassagnau, E. ; Morinière, S. ; Cottier, J.P. ; Faivre, S. ; Barry, B. ; Van den Abbele, T. ; Vulquin, N. ; Lanic, Marie-Delphine ; Babin, E. ; Castain, Claire ; Sudaka, A. ; Bodmer, D. ; Bensadoun, R.J. ; Fieux, Maxime ; Fabiano, E. ; Juliéron, M. ; Maingon, P. ; Rahmani, A. ; Kolb, F. ; Villa, J. ; Mauvais, O. ; Mineur, G. ; Costes-Martineau, Valérie ; Choussy, O. ; J.-M.Prades ; Guillerm, S. ; Lopez, Jonathan ; Galy, C. ; Webert, L. ; Lefevre, M. ; Saroul, N. ; Taouachi, R. ; Baujat, B. ; Page, C. ; Majoufre, C. ; Duflo, S. ; Chabolle, F. ; Uro-Coste, Emmanuelle ; Castelli, J. ; Volondat, M. ; Pissaloux, Daniel ; Ramin, L. ; Badoual, C. ; Vergez, S. ; Cardon, A.Lasne ; Casiraghi, O. ; Molinier-Blossier, S. ; Dufour, X. ; Siegfried, A. ; de Monès, E. ; Dang, N. Pham ; Aubry, K. ; Brenet, E. ; Liem, X. ; Prevost, A. ; Saada, E. ; Franetti, D. ; Ceruse, P. ; Jegoux, F. ; Linassier, C. ; Descotes, Françoise ; Bozec, L. ; Mirghani, H. ; Camby, S. ; Tassart, M. ; Chevalier, D. ; Coste, F. ; Lapierre, A. ; Evrard, C. ; Kaminsky, M.-C. ; Jeanne, C. ; Mouawad, F. ; Costes, V. ; Saint Guily, J. Lacau ; Xu-Shan, S. ; Muller, L. ; Merol, J.-C. ; Alsugair, Ziyad ; J.Thariat ; Moya-Plana, A. ; Patron, V. ; Tirode, Franck ; Maurina, T. ; Vauleon, E. ; David, M. Timar ; Verillaud, B. ; Malouf, G. ; Modesto, A. ; Lapeyre, M. ; Herman, P. ; Leroy, X. ; Digue, L. ; Coste, E. Uro ; Orliac, H. ; Champagnac, Anne ; Dupin, C.

AIMSMost salivary gland neoplasms are distinguished by specific recurrent gene fusions. Recently, a subset of pleomorphic adenomas (PAs) originated from the parotid gland harboring the HMGA2:WIF1 fusion was described with a canalicular adenoma-like morphology and a greater propensity for recurrence and carcinomatous transformation.METHODS AND RESULTSThis study delineates the clinicopathological attributes of 54 cases of PAs exhibiting HMGA2 alterations, predominantly characterized by the HMGA2:WIF1 fusion, alongside a comparative analysis of their morphological and immunohistochemical profiles. The cohort consisted of 23 females and 31 males (n = 54), mean age was 56.7 (25-84), tumors predominantly originated from the parotid gland (94.4%, 51/54), with 3 cases from seromucous glands (5.6%). Mean tumor size was 2.6 cm (0.8-7.5). No clinical difference (demographic, follow-up) was observed among histological subsets (conventional, hybrid, and pure). Complete excision was performed in all cases, with follow-up data available for 41% (22/54) of patients, showing 13.6% of recurrence (3/22) between 5 and 8 months. Various histological growth patterns were identified, with the pure hypercellular monomorphic subset being the most prevalent. The HMGA2:WIF1 gene was identified in all subsets without any particular predominance. Novel gene partners of HMGA2 were identified, comprising NRXN1, INPP4B, MSRB3, PHLDA1, and FLJ41278.CONCLUSIONSThe present study reports that the HMGA2:WIF1 gene fusion was present in all subsets of PAs without significant predominance. However, further investigations are warranted to explore the relationship between histological subsets of PAs and the molecular alterations underlying them.

01 Apr 2024·Journal of Cellular and Molecular Medicine

Autosomal recessive non‐syndromic hearing loss genes in Pakistan during the previous three decades

Review

Author: Shadab, Madiha ; Ejaz, Ahsan ; Abbasi, Ansar Ahmed ; Ben‐Mahmoud, Afif ; Kim, Hyung‐Goo ; Gupta, Vijay ; Vona, Barbara

AbstractHearing loss is a clinically and genetically heterogeneous disorder, with over 148 genes and 170 loci associated with its pathogenesis. The spectrum and frequency of causal variants vary across different genetic ancestries and are more prevalent in populations that practice consanguineous marriages. Pakistan has a rich history of autosomal recessive gene discovery related to non‐syndromic hearing loss. Since the first linkage analysis with a Pakistani family that led to the mapping of the DFNB1 locus on chromosome 13, 51 genes associated with this disorder have been identified in this population. Among these, 13 of the most prevalent genes, namely CDH23, CIB2, CLDN14, GJB2, HGF, MARVELD2, MYO7A, MYO15A, MSRB3, OTOF, SLC26A4, TMC1 and TMPRSS3, account for more than half of all cases of profound hearing loss, while the prevalence of other genes is less than 2% individually. In this review, we discuss the most common autosomal recessive non‐syndromic hearing loss genes in Pakistani individuals as well as the genetic mapping and sequencing approaches used to discover them. Furthermore, we identified enriched gene ontology terms and common pathways involved in these 51 autosomal recessive non‐syndromic hearing loss genes to gain a better understanding of the underlying mechanisms. Establishing a molecular understanding of the disorder may aid in reducing its future prevalence by enabling timely diagnostics and genetic counselling, leading to more effective clinical management and treatments of hearing loss.

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MSRB3

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