Ask about this productRelated genes to: RBMXL2 antibody
- Gene:
- RBMXL2 NIH gene
- Name:
- RBMX like 2
- Previous symbol:
- -
- Synonyms:
- HNRNPG-T, HNRPGT
- Chromosome:
- 11p15
- Locus Type:
- gene with protein product
- Date approved:
- 2007-07-13
- Date modifiied:
- 2018-04-26
Related products to: RBMXL2 antibody
Related articles to: RBMXL2 antibody
- Improvement of protein efficiency (PE) is a key factor for a sustainable pig production, as nitrogen excretion contributes substantially to environmental pollution. Protein efficiency has been shown to be heritable and genetically correlated with performance traits such as feed conversion ratio (FCR) and average daily feed intake (ADFI). This study aimed to identify genomic regions associated with these traits through single-variant genome-wide association studies (GWAS) and regional heritability mapping (RHM) using whole-genome sequence variants from low-pass sequencing of more than 1000 Swiss Large White pigs. - Source: PubMed
Publication date: 2025/08/14
Ewaoluwagbemiga Esther OluwadaLloret-Villas AudaldNosková AdélaPausch HubertKasper Claudia - Previously, we showed that the germ cell-specific nuclear protein RBMXL2 represses cryptic splicing patterns during meiosis and is required for male fertility (Ehrmann et al., 2019). Here, we show that in somatic cells the similar yet ubiquitously expressed RBMX protein has similar functions. RBMX regulates a distinct class of exons that exceed the median human exon size. RBMX protein-RNA interactions are enriched within ultra-long exons, particularly within genes involved in genome stability, and repress the selection of cryptic splice sites that would compromise gene function. The gene is silenced during male meiosis due to sex chromosome inactivation. To test whether RBMXL2 might replace the function of RBMX during meiosis we induced expression of RBMXL2 and the more distantly related RBMY protein in somatic cells, finding each could rescue aberrant patterns of RNA processing caused by RBMX depletion. The C-terminal disordered domain of RBMXL2 is sufficient to rescue proper splicing control after RBMX depletion. Our data indicate that RBMX and RBMXL2 have parallel roles in somatic tissues and the germline that must have been conserved for at least 200 million years of mammalian evolution. We propose RBMX family proteins are particularly important for the splicing inclusion of some ultra-long exons with increased intrinsic susceptibility to cryptic splice site selection. - Source: PubMed
Publication date: 2024/10/02
Siachisumo ChilelekoLuzzi SaraAldalaqan SaadHysenaj GeraldDalgliesh CarolineCheung KathleenGazzara Matthew RYonchev Ivaylo DJames KatherineKheirollahi Chadegani MahsaEhrmann Ingrid ESmith Graham RCockell Simon JMunkley JenniferWilson Stuart ABarash YosephElliott David J - Placental DNA methylation (DNAm) may be a potential mechanism underlying the effects of prenatal bisphenol analogues (BPs) exposure on reproductive health. Based on the Shanghai-Minhang Birth Cohort Study (S-MBCS), this study investigated associations of placental DNAm at reproduction-related genes with prenatal BPs exposure and children's digit ratios at age 4 using multiple linear regression models, and mediation analysis was further used to examine the mediating role of placental DNAm in the associations between prenatal BPs exposure and digit ratios among 345 mother-child pairs. Prenatal exposure to bisphenol A (BPA) was associated with hypermethylation at Protocadherin 8 (), RBMX Like 2 (), and Sperm Acrosome Associated 1 (), while bisphenol F (BPF) exposure was associated with higher methylation levels of Fibroblast Growth Factor 13 (). Consistent patterns were found in associations between higher DNAm at the 4 genes and increased digit ratios. Further mediation analysis showed that about 15% of the effect of BPF exposure on increased digit ratios was mediated by placental methylation. In conclusion, the altered placental DNAm status might be a mediator underlying the feminizing effect of prenatal BPs exposure. - Source: PubMed
Publication date: 2024/06/19
Chen JiaxianZhu HaijunChen YafeiPan ShuqinLiang HongSong XiuxiaWu QihanYuan WeiMiao MaohuaWang Ziliang - Gene expression in meiotic cells in the testis is characterized by intense transcriptional activity and alternative splicing. These processes are mainly controlled by RNA-binding proteins expressed strongly in germ cells. Functional impairments in any of these proteins' functions can lead to defects in meiosis and thus severe male infertility. Here, we have identified a homozygous frameshift mutation (NM_014469.4:c.301dup; p.Ser101LysfsTer29) in the RNA-binding motif protein, X-linked like 2 (RBMXL2) gene in a man with an azoospermia due to meiotic arrest. As RBMXL2 is known to be crucial for safeguarding the meiotic transcriptome in mice testes, we hypothesized that this variant leads to cryptic splice site poisoning. To determine the variant's impact on spermatogenesis, we confirmed the absence of RBMXL2 protein in the patient's testis tissue and then evidenced abnormal expression of several spermatogenesis proteins (e.g. meiosis-specific with coiled-coil domain) known to be altered in rbmxl2 knock-out mice with meiotic arrest. Our results indicate that RBMXL2's function in spermatogenesis is conserved in mammals. We hypothesize that deleterious variant in the RBMXL2 gene can result in male infertility and complete meiotic arrest, due to the disruption of gene expression by cryptic splice site poisoning. - Source: PubMed
Publication date: 2022/09/14
Ghieh FarahIzard VincentPoulain MarineFortemps JohanneKazdar NadiaMandon-Pepin BéatriceFerlicot SophieAyoubi Jean MarcVialard François - High levels of transcription and alternative splicing are recognized hallmarks of gene expression in the testis and largely driven by cells in meiosis. Because of this, the male meiosis stage of the cell cycle is often viewed as having a relatively permissive environment for gene expression. In this review, we highlight recent findings that identify the RNA binding protein RBMXL2 as essential for male meiosis. RBMXL2 functions as a "guardian of the transcriptome" that protects against the use of aberrant (or "cryptic") splice sites that would disrupt gene expression. This newly discovered protective role during meiosis links with a wider field investigating mechanisms of cryptic splicing control that protect neurons from amyotrophic lateral sclerosis and Alzheimer's disease. We discuss how the mechanism repressing cryptic splicing patterns during meiosis evolved, and why it may be essential for sperm production and male fertility. - Source: PubMed
Publication date: 2021/12/20
Aldalaqan SaadDalgliesh CarolineLuzzi SaraSiachisumo ChilelekoReynard Louise NEhrmann IngridElliott David J