ArticleMolecular endocrinology (Baltimore, Md.)2006
Thyroid-specific enhancer-binding protein/NKX2.1 is required for the maintenance of ordered architecture and function of the differentiated thyroid.
Article in Molecular endocrinology (Baltimore, Md.), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 3 of them syntheses that pooled it.
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Who cites it
61 citing papers in PubMed, 3 syntheses or guidelines pooled it.
- Systematic review of thyroid function in NKX2-1-related disorders: Treatment and follow-up.PloS one · 2024Pooled it
- Systematic review of thyroid function in NKX2-1-related disorders: Screening and diagnosis.PloS one · 2024Pooled it
- TITF1 and TITF2 loci variants indicate significant associations with thyroid cancer.Endocrine · 2015Pooled it
- The HEAT Repeat Protein MROH1 Deficiency Leads to Reduced Circulating Thyroid Hormone Levels in Mice.Endocrinology, diabetes & metabolism · 2026Article
- Resolving thyroid lineage cell trajectories merging into a dual endocrine gland in mammals.Nature communications · 2026Article
- Unveiling the rare coexistence: thyroid hemiagenesis and thyroid cancer - case series and comprehensive review.Frontiers in endocrinology · 2026Review
- FoxA1/2-dependent epigenomic reprogramming drives lineage switching in lung adenocarcinoma.Developmental cell · 2025Article
- Maternal Age at Menarche Genes Determines Fetal Growth Restriction Risk.International journal of molecular sciences · 2024Article
- Alveolar epithelial progenitor cells require Nkx2-1 to maintain progenitor-specific epigenomic state during lung homeostasis and regeneration.Nature communications · 2023Article
- NK2 homeobox gene cluster: Functions and roles in human diseases.Genes & diseases · 2023Review
- Tissue specificity of oncogenic BRAF targeted to lung and thyroid through a shared lineage factor.iScience · 2023Article
- Maternal Age at Menarche Gene Polymorphisms Are Associated with Offspring Birth Weight.Life (Basel, Switzerland) · 2023Article
- Transcriptional Circuitry of NKX2-1 and SOX1 Defines an Unrecognized Lineage Subtype of Small-Cell Lung Cancer.American journal of respiratory and critical care medicine · 2022Article
- Article
- FoxA1 and FoxA2 control growth and cellular identity in NKX2-1-positive lung adenocarcinoma.Developmental cell · 2022Article
- Excess neuropeptides in lung signal through endothelial cells to impair gas exchange.Developmental cell · 2022Article
- Modeling Human Thyroid Development by Fetal Tissue-Derived Organoid Culture.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- XB130 Deficiency Causes Congenital Hypothyroidism in Mice due to Disorganized Apical Membrane Structure and Function of Thyrocytes.Thyroid : official journal of the American Thyroid Association · 2021Article
- Differential chromatin binding of the lung lineage transcription factor NKX2-1 resolves opposing murine alveolar cell fates in vivo.Nature communications · 2021Article
- Article
1 more citing papers are in PubMed but not listed here.
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6 authors.
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Abstract
Thyroid-specific enhancer-binding protein (T/ebp)/Nkx2.1-null mouse thyroids degenerate by embryonic day (E) 12-13 through apoptosis whereas T/ebp/Nkx2.1-heterogyzgous mice exhibit hypothyroidism with elevated TSH levels. To understand the role of T/ebp/Nkx2.1 in the adult thyroid, a thyroid follicular cell-specific conditional knockout (KO) mouse line, T/ebp(fl/fl);TPO-Cre, was established that expresses Cre recombinase under the human thyroid peroxidase (TPO) gene promoter. These mice appeared to be healthy and exhibited loss of T/ebp/Nkx2.1 expression in many, but not all, thyroid follicular cells as determined by immunohistochemistry and real-time PCR, thus presenting a T/ebp-thyroid-conditional hypomorphic mice. Detailed analysis of the thyroids from T/ebp(fl/fl), T/ebp(fl/fl);TPO-Cre, and T/ebp(fl/ko) mice, where the latter mouse line is derived from crosses with the original T/ebp/Nkx2.1-heterozygous mice, revealed that T/ebp(fl/fl);TPO-Cre mice can be classified into two groups with different phenotypes: one having atrophic/degenerative thyroid follicles with frequent presence of adenomas and extremely high serum TSH levels, and the other having an altered thyroid structure with reduced numbers of extraordinary dilated follicles consisting of excessive numbers of follicular cells as compared with those usually found in the normal thyroid. The latter phenotype was also observed in aged T/ebp(fl/ko) mouse thyroids. In vitro three-dimensional thyroid primary cultures using thyroids from T/ebp(fl/fl);TPO-Cre, T/ebp(fl/ko), and T/ebp(fl/fl) mice, and the latter treated with recombinant adenovirus with and without Cre expression, demonstrated that only cells from T/ebp(fl/fl) mice without adeno-Cre treatment formed follicular structures. Taken together, these results suggest that T/ebp/Nkx2.1 is required for maintenance of the normal architecture and function of differentiated thyroids.
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