PITX1 antibody - middle region (ARP32340_P050)
- Known as:
- PITX1 (anti-) - middle region (ARP32340_P050)
- Catalog number:
- arp32340_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- PITX1 antibody - middle region (ARP32340_P050)
Related genes to: PITX1 antibody - middle region (ARP32340_P050)
- Gene:
- PITX1 NIH gene
- Name:
- paired like homeodomain 1
- Previous symbol:
- BFT
- Synonyms:
- PTX1, POTX
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-02-27
- Date modifiied:
- 2016-01-27
Related products to: PITX1 antibody - middle region (ARP32340_P050)
Related articles to: PITX1 antibody - middle region (ARP32340_P050)
- The pituitary gland is a master regulator of endocrine and reproductive physiology; however, the lack of physiologically relevant in vitro models in livestock species has limited studies of pituitary development and endocrine function. Although pituitary organoids have been generated from human and mouse pluripotent stem cells, comparable models remain unavailable in large animal species. Here, we established functional pituitary-like organoids from ovine embryonic stem cells (oESCs) using a three-dimensional differentiation strategy. The resulting organoids self-organized into Rathke's pouch-like structures and acquired pituitary progenitor characteristics, as demonstrated by the robust expression of LHX3, PITX1, ISLET1 and PROP1. Compared with conventional two-dimensional differentiation, the organoids displayed enhanced structural organization and improved lineage specification. Notably, the organoids exhibited functional gonadotroph maturation, with GnRH treatment significantly upregulating FSHB and LHB expression, as confirmed by immunohistochemistry, qPCR and Western blot. SMART-Seq transcriptome analysis revealed progressive loss of pluripotency-associated signatures and activation of pituitary developmental programs, including sustained expression of lineage-associated regulators such as PAX6. Collectively, this study establishes the first ovine pituitary-like organoid model and demonstrates its capacity to generate functional GnRH-responsive gonadotroph cells. This platform provides a valuable resource for investigating pituitary development, reproductive endocrinology, livestock fertility, and endocrine disease mechanisms in a large-animal context. - Source: PubMed
Publication date: 2026/07/28
Yang HuaXu HuiLv WenliCai YuLi ShanglaiWan YongjieJitjumnong JakreeLuo XiaojuanWang FengZhang Yanli - Pituitary stem/progenitor cells are essential for regulating the physiological functions mediated by anterior pituitary hormones. Studying the molecular mechanisms governing their differentiation of these cells is crucial for improving the cattle productivity, an agriculturally and industrially important animal. However, elucidating such mechanisms remain a challenge, as maintaining pituitary stem/progenitor cells in vitro is difficult. Here, we attempted to establish immortalized cells for continuous utilization of cattle pituitary stem/progenitor cells. The pituitary stem/progenitor cell marker Sox2 was constitutively expressed in the cattle pituitary gland regardless of age. Calf anterior pituitary cells expressing multiple stem/progenitor cell markers (Sox2, Pitx1, Prrx1, and/or Prop1) were immortalized by introducing temperature-sensitive simian virus 40 large T antigen. Hormonal gene expression was not detected in any cell line. Among these SOX2-positive calf anterior pituitary cell lines, a pituitary-specific marker PROP1-positive cell proliferated when the immortalization was switched on, and differentiated into gonadotroph positive for luteinizing hormone when it was off, a finding supported by the increased expression of transcription factors (Pitx1 and Egr1) that upregulate Lhb expression. However, in this cell line, no changes were observed in the differentiation lineage even when a Notch signaling inhibitor was used. Thus, we established a unique calf anterior pituitary progenitor cell line to study the mechanisms of gonadotroph differentiation. - Source: PubMed
Publication date: 2026/07/31
Iwamoto ChihiroOguchi AiYoshimoto SuzukaHiguchi Masashi - How extracellular matrix organization shapes signaling-associated transcription during skeletal development remains incompletely understood. Using CRISPR-Cas9-edited human urine-derived stem cells, we show that loss of the laminin gene preserves canonical chondrogenic marker induction but impairs three-dimensional spheroid morphogenesis and disrupts pericellular matrix architecture. Bulk RNA sequencing and weighted gene co-expression network analysis identify a -associated transcriptional module enriched for embryonic limb morphogenesis genes, with and as inversely correlated hub genes. Projection onto a human fetal hindlimb atlas localizes / co-expression to the endothelial compartment, while and map to endothelial and chondrocyte populations, respectively, suggesting a spatially organized signaling axis partially conserved in mouse. Pharmacologic β-catenin stabilization partially restores selected module transcripts, and endothelial-conditioned medium selectively rescues and in -KO cultures. Together, these data link -dependent matrix organization to a WNT-associated transcriptional program and identify endothelium as a candidate niche source. - Source: PubMed
Publication date: 2026/07/10
Schulz AlexanderBrockmann Emily MUebe SteffenEkici Arif BThiel Christian T - Shank feathering (ptilopody) in chickens is primarily driven by cis-regulatory variants at the PITX1, TBX5, and CUBN loci. Recent refinement has pinpointed the major PITX1 determinant to an ∼18-kb deletion adjacent to H2AFY, which suppresses distal gene expression by disrupting a chromatin insulator. To evaluate these variants, we surveyed over 20,000 birds from diverse populations and identified an atypical, mild-to-variable shank-feathering phenotype in five Chinese indigenous breeds and one selected line. This phenotype is characterized by sparse, short feathers that do not produce the classic "booted" appearance and has at a low prevalence (0.94%-4.83%). The trait showed no significant association with sex (P > 0.05), ruling out a sex-linked inheritance pattern. Targeted genotyping of the known major-effect variants, including the refined H2AFY deletion, was performed in 153 atypical birds, 190 clean‑legged controls, and representative heavy/moderate-feathered individuals. Our results reveal a widespread genetic decoupling from established models in atypical cohorts. In Xiangdong chickens, 38.1% of feathered individuals lack any of the known mutations including PITX1/H2AFY, TBX5, and CUBN. The TBX5 variant exhibited significant incomplete penetrance (66.7%) and failed to co-segregation with the trait in Xiangdong chickens (P > 0.05). No additive phenotypic effects were observed in individuals harboring multiple variants (Cochran-Armitage trend test, P = 0.842), and the CUBN variant showed no association across the studied populations (P > 0.05). These findings provide quantitative evidence that atypical ptilopody operates under a genetic architecture independent of the established PITX1-TBX5 variants. Our results suggest greater genetic complexity than previously recognized and underscore the potential for discovering alternative regulatory mechanisms within these indigenous populations. - Source: PubMed
Publication date: 2026/07/08
Huang XunheZhang ZhifengZhong ZhipengDu BingwangWu QiongLi Jingyi - Epithelial-to-mesenchymal transition (EMT) is a dynamic process during which cells lose their epithelial characteristics and acquire mesenchymal traits. In cancer, EMT is closely associated with tumor initiation, progression, invasion, metastasis, and therapy resistance. Rather than being a binary state switch, EMT encompasses a spectrum of tumor states with distinct functional properties. However, the transcription factors (TFs) that govern transitions between these EMT states remain poorly defined. Here, using multi-omic approaches combining single-cell RNA-seq and single-cell ATAC-seq, we delineate the transcriptomic and chromatin landscapes of distinct EMT states in a mouse model of skin squamous cell carcinoma (SCC). Through CRISPR/Cas9-mediated loss-of-function studies coupled with in vitro and in vivo functional assays, we identify TFs regulating specific EMT states. Klf5 and Pitx1 control the early stages of EMT and are essential for metastasis formation. In contrast, Nfatc1 and Creb3l1 act at later stages of EMT. Similar EMT states and regulatory patterns are found in mouse pancreatic adenocarcinoma and human cancers. Altogether, our study defines the transcriptional and chromatin landscape controlling EMT progression in mouse skin SCC, identifies EMT state-specific TFs and highlights their essential roles in regulating metastasis. - Source: PubMed
Publication date: 2026/07/11
Pérez-González AndreaWindels GabrielBévant KevinLengrand JustineLemaire SophieMoers VirginieScozzaro SamuelDebroux UlysseDubois ChristineVanuytven SebastiaanBlanpain Cédric