FOXA1 Mouse Monoclonal Antibody
- Known as:
- FOXA1 Mouse Monoclonal Antibody
- Catalog number:
- BIN-003169-M01
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- FOXA1 Mouse Monoclonal Antibody
Related genes to: FOXA1 Mouse Monoclonal Antibody
- Gene:
- FOXA1 NIH gene
- Name:
- forkhead box A1
- Previous symbol:
- HNF3A
- Synonyms:
- -
- Chromosome:
- 14q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-02-11
- Date modifiied:
- 2015-02-02
Related products to: FOXA1 Mouse Monoclonal Antibody
Related articles to: FOXA1 Mouse Monoclonal Antibody
- Non-fibrillar type XVII collagen (COL17A1) is a hemidesmosomal component of the epidermis and a key skin-disease molecule. We previously reported that COL17A1 is expressed in the urothelium of multiple species at low constitutive or in inducible levels. To clarify its function in the ureter, Col17a1-knockout (KO) mice were examined from 2 to 12 weeks of age. After 4 weeks, Col17a1-KO mice showed shorter ureteral length, smaller cross-sectional area, and disorganized urothelial layers compared with wild-type littermates, accompanied by systemic growth retardation. At 4 and/or 12 weeks, Col17a1-KO urothelium exhibited a higher epithelial area ratio, loss of polarity, intraluminal cells, lumen narrowing, and indistinct mucosal folds. Abnormalities were evident as early as 2 weeks, particularly in umbrella cells, which showed altered apical surfaces, hypertrophy, smaller vesicles, and shortened interdigitations. RNA-seq of 2-week-old Col17a1-KO ureters revealed upregulation of immune-related genes and downregulation of epithelial development genes. Uroplakin 2, a key urothelial molecule, was reduced in Col17a1-KO ureters at 1 day and 2 weeks but not at 12 weeks. Its transcription factor, forkhead box protein A1, was persistently reduced, with markedly lower protein expression in umbrella cells. These findings indicate that urothelial COL17A1 is essential for proper urothelial differentiation during postnatal development. - Source: PubMed
Publication date: 2026/04/27
Suzui AmyNamba TakashiHiraishi MasayaOe SaoKira ShunnosukeOtani YukiZhong RuiNatsuga KenIchii Osamu - Breast cancer is posing a serious threat to the health of the female workforce as one of the most prevalent malignancies. Emerging epidemiological evidence suggests that insufficient intake of the trace element, iodine, is associated with breast oncogenesis. In this paper, we propose a potential link between iodine deficiency and increased breast cancer risk. A central element of this mechanism may involve the cytoplasmic mislocalization and oncogenic function of the sodium/iodide symporter (NIS), which primarily mediates iodine transport under physiological conditions in the human body. We propose a three-stage model: (1) Initiation: Iodine deficiency triggers systemic alterations in the hypothalamic-pituitary-thyroid (HPT) and gonadal (HPG) axes, as well as lactogenic signaling, establishing a proliferative and inflamed breast microenvironment. (2) Heterogeneous subtype-specific evolution: For hormone receptor-positive (HR+) breast cancer, sustained PI3K/AKT activation driven by the relative dominance of estrogen disrupts normal glycosylation, leading to the cytoplasmic retention of NIS. For triple-negative breast cancer, and mutations primarily contribute to significant upregulation of NIS. (3) Malignant evolution: Cytoplasmic NIS associates with the leukemia-associated RhoA guanine exchange factor (LARG) and hyperactivates the RhoA-ROCK signaling pathway, driving cytoskeletal rearrangement, tumor invasion and metastasis. Deciphering the contributions of iodine status toward breast carcinoma development is assumed to open new avenues for novel therapeutic measures for breast cancer. - Source: PubMed
Publication date: 2026/04/10
Liu JiaZhou XingtongXu YingZhou YidongSun Qiang - Rathke's cleft cysts (RCCs) are benign cystic lesions of the sellar and suprasellar regions that may cause hypopituitarism and arginine vasopressin (AVP) deficiency when symptomatic. A recent study with Isl-1 knockout mice identified six molecular markers-KRT8, TUBA1A, SOX2, SOX9, FOXA1, and FOXJ1-as potential indicators of RCC pathogenesis. This study aimed to investigate the expression patterns of these markers in human RCCs and examine their association with clinical manifestations. - Source: PubMed
Publication date: 2026/04/24
Sasaki YurikoBando HironoriKanzawa MakiFukuhara NoriakiBrinkmeier Michelle LYamamoto MasaakiUrai ShinMotomura YumaKobatake MasakiOhmachi YukaTsujimoto YasutakaOi-Yo YukaSuzuki MasakiYamamoto NaokiFujita YuichiNishioka HiroshiYamada ShozoFukuoka HidenoriIguchi GenzoCamper Sally AOgawa Wataru - Mutations in BMP4 have been associated with malformations of the urinary tract in human patients. Genetic studies in mice have shown that these defects are linked to the expression of Bmp4 in the mesenchymal primordium of the ureter, where it acts as a critical signal for coordinated cytodifferentiation of the mesenchymal and epithelial tissues. Here, we used unbiased transcriptional profiling of ureters with genetic depletion of Bmp4 and pharmacological inhibition of BMP4 signaling to decipher the gene regulatory network controlled by BMP4 in the early ureter, focusing on transcription factors as possible drivers of cytodifferentiation. We show that in Bmp4-deficient ureters, expression of Grhl3, Msx2, Pparg, Trp63 and Foxa1 in the epithelial compartment, and of Gata6, Hopx, Id2, Id4, Myocd, Snai1 and Tbx18 in the mesenchymal primordium is reduced. Expression of Msx2, Pparg, Gata6, Id genes, Tbx18 and Snai1 requires direct BMP4 signaling input, whereas reduced expression of the other genes is likely due to secondary changes, including increased retinoic acid signaling. Conditional gene targeting of Smad4 revealed that BMP4-dependent activation of transcription factor genes is mediated in part by SMAD effectors in both ureteral tissues. Thus, our work links BMP4 (signaling) to known transcriptional regulators of ureteral cytodifferentiation and uncovers additional factors that may be relevant to this program. - Source: PubMed
Publication date: 2026/04/22
Deuper LenaHense NicolasBeckers AnjaThiesler HaukeMamo Tamrat MBergmann FlorianHildebrandt HerbertTrowe Mark-OliverKispert Andreas - B7-H3 (CD276) represents a promising therapeutic target tested in high-risk localized and treatment-refractory metastatic prostate cancer (PC). To guide therapeutic development and treatment strategies, we examined prostate tumors and evaluated expression, molecular features, and overall survival (OS), accounting for tissue site, hormone-sensitivity status, and race. - Source: PubMed
Publication date: 2026/04/21
Makovec AllisonGustafson Ava PGandhi NishantRampalli SwatiArafa Ali TElliott AndrewSmith NormFelices MartinKennedy Philippa RShenderov EugenePatnaik AkashNarayan VivekHeath Elisabeth IZorko Nicholas AShi XiaoleiAntonarakis Emmanuel SMcKay Rana RHwang Justin