PTF1A antibody - N-terminal region (ARP32531_P050)
- Known as:
- PTF1A (anti-) - N-terminal region (ARP32531_P050)
- Catalog number:
- arp32531_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- PTF1A antibody - N-terminal region (ARP32531_P050)
Related genes to: PTF1A antibody - N-terminal region (ARP32531_P050)
- Gene:
- PTF1A NIH gene
- Name:
- pancreas associated transcription factor 1a
- Previous symbol:
- -
- Synonyms:
- PTF1-p48, bHLHa29, p48
- Chromosome:
- 10p12.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-04
- Date modifiied:
- 2018-02-20
Related products to: PTF1A antibody - N-terminal region (ARP32531_P050)
Related articles to: PTF1A antibody - N-terminal region (ARP32531_P050)
- Bergmann glia (BG) are a specialized glial population essential for cerebellar development, yet their developmental timeline and molecular identity in the human cerebellum remain poorly understood. Here, we combined detailed histopathological analysis with spatial transcriptomics and single-nucleus RNA sequencing to generate a developmental atlas of human cerebellar BG. Histology revealed that BG emerge around 11 postconception weeks (PCW), initially serving as a scaffold for Purkinje cells (PCs) migrating into the PC layer of the cerebellar cortex. Following the establishment of a multilayered PC arrangement, BG form a distinct parallel layer separated from the PCs by the lamina dissecans (LD), with both layers merging in the third trimester. This developmental sequence challenges earlier studies that suggested BG appear late in the third trimester. Comparative histology in mice, ferrets, and marmosets indicates that this trilaminar organization, including the LD, is likely unique to humans. Integration of spatial and single-nucleus transcriptomic datasets identified an ventricular zone progenitor cluster giving rise to BG, astrocytes, and oligodendrocytes. Pseudotime analyses delineated three gliogenic lineages and revealed two temporally and transcriptionally distinct BG populations, emerging at 11-12PCW and 17PCW, suggesting multiphasic BG ontogeny. Together, these multimodal data link cellular lineage, spatial organization, and molecular identity of human cerebellar glia, providing a framework for future studies on the role of BG in cerebellar function and their potential contributions to vulnerability in neurodevelopmental disorders. - Source: PubMed
Publication date: 2026/02/10
He GuanyiDu SimonTan HenryYellampally SriErickson Anders WFernandez VirginiaEncha-Razavi FerechtePhillips Kimberley AHaberler ChristineAmberg NicoleBorrell VictorNorthcott Paul ATaylor Michael DMillen Kathleen JHaldipur Parthiv - Dietary macronutrient composition has emerged as a key modulator of pancreatic tumorigenesis, yet the impact of lipid-rich diets, particularly ketogenic diets (KD) on the earliest stages of pancreatic cancer development remains unclear. To investigate how dietary lipids shape the initiation and progression of Kras-driven neoplasia, we examined the effects of low-fat diet (LFD), high-fat diet (HFD), and KD in the mouse model. KD-fed mice showed the shortest survival (median 26 ± 7 days) compared with SD (87 ± 29; p = 0.02) and LFD (57 ± 27; p = 0.02), while HFD-fed mice also exhibited reduced survival relative to SD (35 ± 25; p = 0.05). KD feeding induced severe glucose intolerance and elevated circulating β-hydroxybutyrate levels. Histologically, KD-fed mice developed invasive, sarcomatoid-like pancreatic ductal adenocarcinoma (PDAC), while HFD-fed mice showed increased poorly differentiated PDAC; in both groups these aggressive tumors were associated with extensive fibrosis and increased stromal CD39 expression relative to tumor compartments. Proteomic analysis demonstrated activation of PI3K-Akt-mTOR and EGFR signaling in KD and HFD-fed mice. Serum cytokines/chemokines profiling revealed pro-inflammatory and pro-angiogenic milieu in KD-fed mice. Collectively, these results show that dietary lipid enrichment prior to oncogenic Kras activation may accelerate early pancreatic neoplasia and foster a microenvironment conducive to tumor progression. These findings underscore the need for careful consideration of KD use in individuals at elevated risk for pancreatic cancer. - Source: PubMed
Publication date: 2025/12/01
Sardarni Urvinder KaurFaraoni Erika YWaller Alyssa MStrickland Lincoln NO'Brien BayleeCox Jesse LMcAllister FlorenciaBailey-Lundberg Jennifer M - Patients with chronic pancreatitis (CP) have a higher risk of developing pancreatic ductal adenocarcinoma (PDAC). Although pancreatitis has been found to promote PDAC initiation and progression, its role in PDAC tumorigenesis remains poorly understood. - Source: PubMed
Publication date: 2026/01/19
Ma ZhilongDong MingweiPan HaoqiXu JunyiLuo TingyiXie WangchengXiao MingmingWen XinHua JieQian DaohaiMeng QingcaiWang YufengWu DiZhang XiaobingYang TingsongSong ZhenshunWang WeiXu JinYu XianjunShi Si - A Japanese boy carried a paternally inherited single-nucleotide deletion in PTF1A exon 1 (c.775delC) and a maternally inherited nucleotide substitution in the distal enhancer region (g.23508356T>G). Both variants were hitherto unreported. The patient exhibited transient anemia in addition to typical clinical features of pancreatic hypoplasia, but no neurodevelopmental abnormalities. These results highlight the clinical importance and broad mutation spectrum of PTF1A variants as a cause of pancreatic hypoplasia. In addition, our data imply that phenotypes of PTF1A abnormalities are variable and include etiology-unknown transient anemia. - Source: PubMed
Publication date: 2026/01/15
Aramaki MichihikoDoi HibikiKato-Fukui YukoKoga NobuhikoKashimada KenichiFukami Maki - Pancreatic ductal adenocarcinoma (PDAC) is known to develop through a stepwise progression from precursor lesions, such as pancreatic intraepithelial neoplasias (PanIN). An alternative carcinogenic pathway has been proposed via transformation of acinar cells, with development of acinar-ductal metaplasia (ADM) and atypical flat lesions (AFL). Defining the characteristics of PDAC precursors is crucial to better understand PDAC carcinogenesis. - Source: PubMed
Publication date: 2026/01/13
Yavas AslihanBoshoven LeonHorny KaiHaensch SebastianGoering WolfgangSchlensog MartinHaeberle LenaEsposito Irene