NKX2-5

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NKX2-5

A gene on chromosome 5q34 that encodes a homeobox transcription factor implicated in commitment to, and/or differentiation of, the myocardial lineage. It acts as a transcriptional activator of ANF in co-operation with GATA4.

Molecular pathology
NKX2-5 mutations cause atrial septal defect with atrioventricular conduction defect, tetralogy of Fallot, and congenital hypothyroidism non-goitrous type 5.
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References in periodicals archive ?
The following markers were used to determine differentiation efficiency: brachyury (R&D Systems) for mesoendoderm, Nkx2.5 (Abcam) for cardiac mesoderm, Nkx2.5 and Isl1 (Developmental Studies Hybridoma Bank) for cardiac progenitors, cTnT (Thermo Fisher Scientific) for cardiomyocytes, double staining of FOXA2 (GeneTex) and SOX17 (GeneTex) for endoderm, CDX2 (GeneTex) for mid/hindgut, Otx2 (R&D Systems) for day 5 neural induction, and PAX6 (GeneTex) for neuroepithelium [17-20].
Figure 9 indicates Gata4 and NKx2.5, as two factors that characterize cardiogenic differentiation.
Cells subjected to cyclic strain expressed GATA-4, [beta]-MHC, NKx2.5, and MEF2c.
In addition, mutations in genes FOXE1, PAX8, TSHR, NKX2.1, or NKX2.5 associated with TD were identified in only 2-3% of TD cases [15].
In addition, the C allele generates a new binding site to transcription factor Nkx2.5 (YBYCACT TSM) that could favor raet1e gene expression only in positive cells for Nkx2.5 protein (Figure 1(d)).
We also included potential upstream genes such as Csf1r [30], Gata4, Nkx2.5, and Tbx5 [31].
It's called Nkx2.5 and it is found in an emu embryo, where it causes "wing reductions," according to a study in the journal (https://www.nature.com/articles/s41467-017-00112-7) Nature Communications.
However, the etiology of TD is still unclear but can be explained on a small scale by genetic mutations in 4 transcription factors (FOXE1 [5], NKX2.1 [6], PAX8 [7, 8], and NKX2.5 [9]) and at the thyrotrophin receptor [10], which are genes important in the development and normal function of the thyroid gland [11-13].
Ascorbic acid [82] increased the expression of cardiac muscle genes, such as GATA4, Nkx2.5, [alpha]-MHC, [beta]- MHC, and atrial natriuretic factor (ANF), with subsequent cardiac- specific protein production.
Zuo, "Hexabromocyclododecane exposure induces cardiac hypertrophy and arrhythmia by inhibiting miR-1 expression via up-regulation of the homeobox gene Nkx2.5," Journal of Hazardous Materials, vol.
The transcription factors GATA-4, Nkx2.5, [alpha]-MHC in TGF-[beta]1 treated cells were assessed by semi-quantitative RT-PCR on day 7, 14, or 28.
Although iPSC-CMs express relevant ion channel genes (SCN5A, KCNJ2, CACNA1C, KCNQ1, and KCNH2), structural genes (MYH6, MYLPF, MYBPC3, DES, TNNT2, and TNNI3), and transcription factors (NKX2.5, GATA4, and GATA6) [77], they differ from adult ventricular cardiomyocytes in a number of properties.