Ask about this productRelated genes to: LEFTY2 Blocking Peptide
- Gene:
- LEFTY2 NIH gene
- Name:
- left-right determination factor 2
- Previous symbol:
- TGFB4, EBAF
- Synonyms:
- LEFTA, LEFTYA
- Chromosome:
- 1q42.12
- Locus Type:
- gene with protein product
- Date approved:
- 1998-01-20
- Date modifiied:
- 2016-10-05
Related products to: LEFTY2 Blocking Peptide
Related articles to: LEFTY2 Blocking Peptide
- Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that western blot data shown in Fig. 1C on p. 1232 were strikingly similar to data in a paper that had previously been published in the journal that was written by different authors at different research institutes. Upon performing an independent analysis of the data in this paper in the Editorial Office, it also came to light that the cellular images featured in Fig. 6B on p. 1233 had also previously appeared in another article published in the journal that was similarly written by different authors at different research institutes. Given that the abovementioned data had already been published before the receipt of this paper at , the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Molecular Medicine 42:1229‑1236, 2018; DOI: 10.3892/ijmm.2018.3703]. - Source: PubMed
Publication date: 2026/06/05
Gao XiaoxuCai YanAn Ruifang - The Y chromosome harbors few protein-coding genes, and their roles in early human development remain largely unclear. Here, we demonstrate that UTY, a Y-linked homolog of the histone demethylase UTX, plays a crucial demethylase-independent role in maintaining pluripotency in human embryonic stem cells (hESCs). Despite its low expression and weak enzymatic activity, UTY co-occupies cis-regulatory elements with UTX and promotes transcription of key pluripotency genes, including NODAL, LEFTY1 and LEFTY2. Integrated analyses of single- and double-knockout hESCs reveal that UTY and UTX function redundantly to maintain chromatin accessibility and ensure proper recruitment of core transcription factors such as OCT4 and SOX2. The combined loss of UTY and UTX disrupts transcription factor localization, induces widespread gene expression changes and leads to a collapse of the pluripotent state, without detectable changes in H3K27 methylation. Instead, these defects are associated with impaired recruitment of ATP-dependent chromatin remodelers and reduced histone acetylation, suggesting a demethylase-independent mechanism. Our findings uncover an essential role for the evolutionarily conserved UTY in safeguarding enhancer function and transcription factor occupancy, highlighting Y-linked regulatory mechanisms crucial for human pluripotency. - Source: PubMed
Publication date: 2026/05/14
Akiyama TomohikoNakahara ToshiyaSato SaekoIshiguro Kei-IchiroYukawa MasashiYamamoto MiuTakahashi HidehisaKo Minoru S H - WNT, BMP, FGF, and Nodal signalling gradients drive naive to primed epiblast transitions and primitive endoderm specification, as well as subsequent gastrulation of the implanted embryo. Recently, these pathways were shown to control a signalling rheostat that modulates chromosome replication and segregation fidelity in human pluripotent stem cells. In particular, WNT and BMP antagonists associated with embryo anteriorization during gastrulation (DKK1, Cerberus, LEFTY2, Noggin, and Chordin) induce DNA replication stress and damage in S-phase leading to ultra-fine-bridges and whole-chromosome mis segregation in the subsequent mitosis. Of note, aneuploidy in pre- and early post-implantation embryos is the first cause of miscarriage in humans, and has also been associated with neurodevelopmental disorders. Here, we hypothesize that the antero-posterior (A-P) signalling gradient generates overlapping patterns of genome and chromosomal mosaicism in human embryos, with potential links to human infertility and lineage-specific developmental disorders. - Source: PubMed
Acebrón Sergio PHattemer JaninaRausch TobiasDe Jaime-Soguero Anchel - Exfoliation syndrome (XFS) is characterized by deposition of exfoliation material (XFM) in the anterior segment. XFM contributes to development of exfoliation glaucoma (XFG). Here, we evaluated left-right determination factor 2 (LEFTY2), a TGFβ superfamily protein, as an XFS and XFG biomarker. - Source: PubMed
Smith Andrew J OSheybani ArshamGreenwood MichaelSieck ErinTsai LindaLiu JamesSiegfried CarlaLiu YingShui Ying-BoGonzalez LillyStamer W DanielBassnett Steven - Semen quality serves as a vital indicator of male fertility, yet its underlying genetic and regulatory mechanisms remain poorly understood. Here, 1.15 million records of six semen quality traits from 14 210 boars in four distinct breeds were collected. These traits have low to moderate heritability (0.12-0.26), and are genetically correlated with growth traits like average daily gain. Genome-wide association study (GWAS) and multi-breed meta-analysis detected 234 loci associated with semen quality. Systematic integration of the Pig Genotype-Tissue Expression resource with these GWAS loci allowed the prioritization of 93 causal variants targeting 134 genes. For instance, the expression quantitative trait loci (eQTL) of NAXE in multiple tissues were colocalized with a GWAS loci of the number of sperms, while eQTL of LEFTY2 in the testis was exclusively colocalized with in a GWAS loci of semen volume. Through examining GWAS of semen quality traits in cattle and human complex traits, the ortholog genes (e.g., AURKAIP1 and ADRA2A) significant in pigs also regulated bovine semen quality, and were significantly enriched for heritability of human birth weight and height. This study provides novel insights into semen quality traits in mammals, which will provide candidate genes for pig selective breeding and potential targets for human male infertility research. - Source: PubMed
Publication date: 2026/01/08
Lin QingCai XiaodianZhong ZhanmingLi TingtingChen XinyouAyalew WondossenXu ZhitingWei ChenZhang XiaokeCheng HongZhang ZhenyangLi XuehuaTang YongjieChen SiqianZhou JunSi JingleiWu XiboNing ChaoWang QishanPan YuchunGao YahuiLi JiaqiYu YingZhang ZheZhao YunxiangFang LingzhaoZhang Zhe