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We observed that hyaline membrane disease is the most common cause of perinatal death among respiratory disorders, and in this disease, the expression of TTF-1 is significantly reduced in terminal bronchioles, distal airways, and alveoli compared to the control group.
NKX2-1 expression was upregulated in never-smokers , lung adenocarcinoma and patients with wild-type TP53. A negative correlation between NKX2-1 and miR-365 expression was found but there was no correlation between NKX2-1 and miR-33a expression. NKX2-1 expression impacts prognosis in early-stage non-small cell lung cancer patients, particularly in those with neither TP53 nor KRAS mutations.
Study shows that that NKX2-1 directly and positively regulates transcription of cyclin D1 in lung adenocarcinoma. Also, the expression of NKX2-1, but not cyclin D1, is significantly associated with metastatic incidence as an independent good prognostic factor of adenocarcinoma.
Case Report: TTF-1 expression in of a soft tissue metastasis of mediastinal non-functioning paraganglioma.
Loss of NKX2-1 is associated with cancer.
TTF-1 might be involved in lymph node metastasis of ovarian carcinomas in the presence of lymphangiogenesis
results indicate that TTF-1 expression in NECs suggests a possible role in their normal development and differentiation
Combined genomic and proteomic analyses demonstrated infrequent alteration of validated lung cancer targets but identified novel potential targets for TTF1-negative LUAD, including KEAP1/Nrf2 and DNA repair pathways
Low expression levels of TTF-1 is associated with lung adenocarcinoma.
Immunohistochemical comparison of two TTF-1 mAbs in atypical squamous lesions and sarcomatoid carcinoma of the lung, and pleural malignant mesothelioma suggest possibility for diagnostic errors.
Because TTF-1 is not detected in the vast majority of cases using a separate antibody clone, 8G7G3/1, we conclude that aberrant staining is due to cross-reactivity to unknown antigen(s). TTF-1 positivity and even Napsin A positivity, therefore, cannot be used as conclusive evidence of pulmonary origin and gastrointestinal origin must be considered in the differential diagnosis
CK7, TTF-1 and napsin A are predominantly expressed in primary lung adenocarcinoma patients, with CDX-2 being inconsistently expressed.
Study showed that TTF1 expression was upregulated in tumor tissues from patients with hepatocellular carcinoma (HCC) and that TTF1 mRNA levels were significantly associated with poor prognoses. Moreover, upregulation of TTF1 was shown to promote the proliferation of HCC cells in vitro.
P-AKT and TTF-1 using IHC had statistically significant correlation with EGFR mutation with high negative predictive value
TTF-1 positivity does not exclude the diagnosis of primary Olfactory neuroblastoma, although usually only a small percentage of cells are positive.
TTF-1 immunoreactivity was seen in 19 pulmonary neuroendocrine carcinoma (PNEC) cases (95%) and 13 thymic (TNEC) cases (59.1%). TTF-1 positivity was associated with high sensitivity but low specificity for PNEC, and adding PAX8 negativity significantly increased the specificity. PAX8 positivity alone showed essentially 100% specificity and 86.4% sensitivity for TNEC.
Studied the prognostic relevance of thyroid transcription factor 1 (TTF1) copy number alterations (CNAs) and expression levels in non-small cell lung cancer; found TTF1 CNAs and expression high within tumors and between primary and metastatic tumors.
findings proved that iodinated TG in thyroid follicular lumen regulated TTF-1 and PAX8 expression through thyroid stimulating hormone/thyroid stimulating hormone receptor (TSH/TSHR) mediated cAMP-PKA and PLC-PKC signaling pathways.
it may be useful to combine NAPA and TTF-1 for increased sensitivity in lung cancer diagnostics. There is no substantial difference between monoclonal and polyclonal p40 and between different NAPA clones, whereas there is a difference between the TTF-1 clones 8G7G3/1 and SPT24
TTF-1 shows significant potential as a diagnostic marker to differentiate metastatic pulmonary from non-pulmonary adenocarcinomas in pleural or other effusions.
Nkx2.1 regulates astrogliogenesis of the telencephalon from embryonic day (E) 14.5 to E16.5. Nkx2.1 controls astroglial production spatiotemporally in embryos by regulating proliferation of the contributing Nkx2.1-positive precursors.
NKX2-1 is required in the embryonic septum for cholinergic system development, learning, and memory.
Our findings demonstrate that NKX2-1 overexpression converts AFE to thyroid epithelium in a developmental time-sensitive manner and suggest a general methodology for manipulation of cell-fate decisions of developmental intermediates.
NKX2-1 binding at distal regulatory elements led to a repressed epigenetic state and transcriptional repression in the ventricular zone. Conversely, NKX2-1 is required to establish a permissive chromatin state and transcriptional activation in the sub-ventricular and mantle zones.
Study shows that within the NANCI-Nkx2.1 duplex, NANCI plays an essential role in regulating tissue identity by acting as a transcriptional rheostat to buffer Nkx2.1 expression. During lung development and in adult lung homeostasis, NANCI acts in cis to positively regulate Nkx2.1, and, in turn, Nkx2.1 directly inhibits NANCI expression.
data indicate that TTF-1 interacts with PPFP to inhibit the pro-adipogenic response to pioglitazone, and that the ability of pioglitazone to decrease TTF-1 expression contributes to its pro-adipogenic action.
Identify regulatory link between Nkx2-1, miR-200c, and the transcription factors Nfib and Myb, adding new players to the regulatory mechanisms driven by Nkx2-1 in lung epithelial cells that may have implications in lung development and tumorigenesis.
A population of neural stem cells in the ventral region of the adult ventricular-subventricular zone expresses the transcription factor Nkx2.1 and is derived from Nkx2.1-expressing (Nkx2.1+) embryonic precursors.
We conclude that a dedicated subset of VMHVL neurons marked by ERalpha, NKX2-1, and Tac1 regulates estrogen-dependent fluctuations in physical activity and constitutes one of several neuroendocrine modules that drive sex-specific responses.
Prototypic GPe neurons derive from the medial ganglionic eminence of the embryonic subpallium and express the transcription factor Nkx2-1. These neurons fire at high rates during alert rest, and encode movements through heterogeneous firing rate changes.
Molecular characterization of disseminated tumor cells indicates that downregulation of the transcription factor Nkx2-1 precedes lung adenocarcinoma dissemination.
The Nkx2-1-mediated pathway in the DMH and LH stimulates skeletal muscle function via the sympathetic nervous system and maintains youthful physiology, contributing to the delay in aging and life span extension.
MicroRNA-33a mediates the regulation of high mobility group AT-hook 2 gene (HMGA2) by thyroid transcription factor 1 (TTF-1/NKX2-1).
A review of recent findings with special attention given to the role of NKX2-1 in lung development and carcinogenesis.
Apc and TGF-beta signaling have roles in regulating the key transcriptional factor, Nkx2.1, for lung epithelial progenitor cell fate determination
Nkx2-1 is likely to maintain pulmonary identity by recruiting transcription factors Foxa1 and Foxa2 to lung-specific loci.
Mouse models of bronchopulmonary dysplasia showed reduced levels of TTF-1 and increased levels of vimentin.
Sox2 contributes to Nkx2.1 expression in early mouse development, thus participating in the region-specific activation of Shh, thereby mediating ventral telencephalic patterning induction.
Haploinsufficiency of Nkx2-1 in combination with oncogenic Kras(G12D) caused pulmonary tumors in mice that were phenotypically similar to human mucinous adenocarcinomas.
Grhl2 and Nkx2-1 bind to each other's promoter in vivo, forming a positive feedback regulatory loop.
This studt demonistrated that the expression of Nkx2.1 is restricted to the medial prominence in dogfish.
There exists cooperation between Nodal and Hedgehog pathways in the maintenance of the anterior-dorsal hypothalamus.
hhex, nk2.1a, and pax2.1 regulate thyroid growth and differentiation downstream of Nodal-dependent transcription factors.
This gene encodes a protein initially identified as a thyroid-specific transcription factor. The encoded protein binds to the thyroglobulin promoter and regulates the expression of thyroid-specific genes but has also been shown to regulate the expression of genes involved in morphogenesis. Mutations and deletions in this gene are associated with benign hereditary chorea, choreoathetosis, congenital hypothyroidism, and neonatal respiratory distress, and may be associated with thyroid cancer. Multiple transcript variants encoding different isoforms have been found for this gene. This gene shares the symbol/alias 'TFF1' with another gene, transcription termination factor 1, which plays a role in ribosomal gene transcription.
NK-2 homolog A
, homeobox protein NK-2 homolog A
, homeobox protein Nkx-2.1
, thyroid nuclear factor 1
, thyroid transcription factor 1
, homeodomain protein NKx2.1
, NK2 homeobox 1
, thyroid-specific enhancer-binding protein
, thyroid transcription factor 1 TTF-1 NK-2
, thyroid transcription factor-1
, thyroid transcription factor 1a
, Homeobox protein Nkx-2.1
, LOW QUALITY PROTEIN: homeobox protein Nkx-2.1
, Thyroid nuclear factor 1
, Thyroid transcription factor 1