Ask about this productRelated genes to: PBX1 antibody
- Gene:
- PBX1 NIH gene
- Name:
- PBX homeobox 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1990-09-10
- Date modifiied:
- 2016-05-17
Related products to: PBX1 antibody
Related articles to: PBX1 antibody
- PLAG1 gene fusions have been identified in a subset of uterine sarcomas and were historically associated with myxoid morphology. However, recent evidence shows that not all cases demonstrate myxoid features or conventional smooth muscle immunophenotype. Herein, we present 11 cases of PLAG1-rearranged uterine mesenchymal tumours to further characterize their clinicopathologic, immunohistochemical and molecular profiles. - Source: PubMed
Publication date: 2026/04/22
Cai MengyuanZuo KeYu LinCheng YufanBi RuiGe HuijuanYang WentaoTu Xiaoyu - Chronic stress (CS) exacerbates anxiety and hyperglycemia, emerging as a key risk factor for type 2 diabetes, yet the mechanism remains unclear. Here, we found that CS induces hyperglycemia and enhanced amygdaloid astrocytic senescence in mice. The amygdaloid astrocytic senescence was mediated by the reduction of hexokinase 2 (HK2) driven by pre-B cell leukemia homeobox transcription factor 1 (PBX1). The astrocytic Hk2 deletion mice and amygdala-specific astrocytic Hk2 knockdown mice both display anxiety-like behaviors and hyperglycemia. The reduction of HK2 in astrocytes reduces L-serine synthesis and decreases the supply to neurons for the generation of D-serine by disrupting the astrocyte-neuron serine shuttle. Reduced neuronal D-serine level in the amygdala impaired the balance of sympathetic and parasympathetic amygdala-pancreas projections, leading to hyperglycemia. L-serine supplementation or dasatinib/quercetin administration to eliminate senescent cells alleviates both CS-induced neurobehaviors and peripheral hyperglycemia. Together, these findings reveal that HK2 in amygdaloid astrocytes mediates CS-induced neurobehaviors and hyperglycemia. - Source: PubMed
Publication date: 2026/04/03
He AojieZhu YufeiLiang ChensiHuang ShangmengYuan ZiqiYang ShangchenChen YaoyiCan DanLei AiyuLi HuifangLeng LigeZhang Jie - PBX1-associated congenital anomalies of the kidney and urinary tract syndrome with or without hearing loss, abnormal ears, or developmental delay (CAKUTHED) is a highly pleiotropic, autosomal dominant developmental disorder. The disease spectrum is broad, and only a limited number of prenatal cases have been reported to date. We report two well-documented prenatal cases of CAKUTHED presenting with cardiovascular defects as the initial manifestation in the second trimester. Trio exome sequencing identified two de novo variants in PBX1 (c.192-3C>A and c.869G>A), confirming the genetic diagnosis of CAKUTHED in the two fetuses. In Case 1, minigene assays validated that the c.192-3C>A variant interfered with RNA splicing. The individual predominantly manifested tetralogy of Fallot and renal hypoplasia. In Case 2, the c.869G>A missense variant was identified, with more complex clinical features. Cardiac malformations included coarctation of the aorta, pulmonary artery stenosis, coronary sinus dilatation, and persistent left superior vena cava. Moreover, the fetus exhibited severe growth restriction, polyhydramnios, and marked thoracic and pulmonary defects, with no significant structural abnormalities of the urinary system detected. Both pregnancies were subsequently terminated. Our report, by detailing the previously rarely reported prenatal clinical features and novel genetic variants, helps to expand the known phenotypic and genotypic spectrum of PBX1-related disorders. - Source: PubMed
Publication date: 2026/04/03
Lan ZhuXu BochengWang HaoLiu ShanlingWang HeZhang Zhu - To understand how genes are regulated it is important to assess the molecular basis of TFs cooperation in promoter and enhancer regulatory elements. Compelling genetic, genomic and biochemical data in mammals and zebrafish point at DECA-CCAAT composite elements as important for regulation of gene expression in development. DECA is recognized by the homeodomain (HD) heterodimeric TALE TFs (PBX/PREP), CCAAT by the NF-Y trimer. Both are evolutionarily conserved in eukaryotes, including plants. Sp2, a member of the Sp/KLF family, potentiates association of TALE and NF-Y on DNA. We applied AlphaFold to infer the structural basis of the hexameric complex with DNA. The resulting models position TALE and NF-Y on the respective sites, predicting the complex arrangement of the MEINOX/PBC heterodimerization module of the TALE TFs and the sequence-specific DNA contacts of the HDs to DECA. The complex is tied by the Sp2 N-terminus, which contacts the TALE dimer through the α-helical SP-box and the NF-Y trimer through a novel short linear motif (YA-SLiM). A flexible linker separates the anchor points, consistent with the constrained stereo-alignment of the DECA-CCAAT motif. The models are confirmed by assembly of the recombinant NF-Y/TALE/Sp2 in complex with DNA in vitro. Mutagenesis confirms the importance of the SP-box and YA-SLiM for cooperativity. Rationalising available genomic and biochemical data, the structural models depict a novel mode of cooperative binding on DNA, providing important clues as to how TFs potentially function beyond DECA-CCAAT in different eukaryotic contexts. - Source: PubMed
Publication date: 2026/03/13
Bernardini AndreaGnesutta NerinaMantovani Roberto - OBJECTIVE：To explore the clinical characteristics and genetic etiology of a child with CAKUTHED syndrome. - Source: PubMed
Tang JiaoZhang ChuanYang RuiqiongTian XinyuanZhou BingboWang YupeiHui Ling