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Cat.No.: F4584
| Dilution |
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|
| Application |
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| WB, IP, IHC, IF, FCM |
| Reactivity |
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| Human, Mouse, Rat |
| Source |
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| Rabbit Monoclonal Antibody |
| Storage Buffer |
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| PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3 |
| Storage (from the date of receipt) |
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| -20°C (avoid freeze-thaw cycles), 2 years |
| Predicted MW |
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| 44, 46 |
| Positive Control | Mouse pancreas; Human pancreas; β-TC-6 cells; NIT-1 cells; INS-1 cells |
|---|---|
| Negative Control | mIMCD3 cells |
| Specificity |
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| NKX6.1 Antibody [N24F3] detects endogenous levels of total NKX6.1 protein. |
| Clone |
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| N24F3 |
| Synonym(s) |
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| Homeobox protein Nkx-6.1; Homeobox protein NK-6 homolog A; NKX6-1; NKX6A |
| Background |
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| NKX6.1 is a homeodomain-containing transcription factor essential for pancreatic β-cell development and identity. It contains a conserved 60-amino-acid homeodomain, consisting of three α-helices, with helix III specifically recognizing TAAT-core motifs flanked by distinct nucleotides in target gene promoters. NKX6.1 also features an N-terminal transcriptional repression domain and a C-terminal β-interaction domain (BID), which together enable activation, autoregulation, and interactions with cofactors such as Pdx1, Pax4, and MafA. Expressed in multipotent pancreatic progenitors, NKX6.1 drives endocrine lineage commitment by directly repressing acinar fate genes such as Ptf1a and activating β-cell-specific transcription factors (e.g., Hnf1α, Mnx1, Rfx6) as well as metabolic genes (such as Glut2, G6pc2, Slc30a8, and Ero1lb). This is accomplished through chromatin looping and recruitment of coactivators. NKX6.1 maintains mature β-cell function by supporting glucose-stimulated insulin secretion (GSIS), potentiated by VGF/TLQP-21 and Nr4a1/Nr4a3-mediated proliferation, while concurrently suppressing glucagon (Gcg) expression and epithelial-mesenchymal transition to prevent dedifferentiation. In Notch-repressed trunk progenitors, NKX6.1 is critical for sustaining β-cell mass and identity after birth. Loss of NKX6.1 function leads to β-to-α/δ cell transdifferentiation, hyperglycemia, and diabetes mellitus. Conversely, NKX6.1 overexpression can enhance β-cell proliferation and GSIS, but may also increase the risk of tumorigenesis through dysregulation of Nr4a and c-Fos signaling pathways. |
| References |
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