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NKX6.1 Antibody [N24F3]

Cat.No.: F4584

    Application: Reactivity:
    • F4584-wb
      Lane 1: INS-1

    Usage Information

    Dilution
    1:1000
    1:50
    1:3200
    1:400
    1:200
    Application
    WB, IP, IHC, IF, FCM
    Reactivity
    Human, Mouse, Rat
    Source
    Rabbit Monoclonal Antibody
    Storage Buffer
    PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3
    Storage (from the date of receipt)
    -20°C (avoid freeze-thaw cycles), 2 years
    Predicted MW
    44, 46
    Positive Control Mouse pancreas; Human pancreas; β-TC-6 cells; NIT-1 cells; INS-1 cells
    Negative Control mIMCD3 cells

    Datasheet & SDS

    Biological Description

    Specificity
    NKX6.1 Antibody [N24F3] detects endogenous levels of total NKX6.1 protein.
    Clone
    N24F3
    Synonym(s)
    Homeobox protein Nkx-6.1; Homeobox protein NK-6 homolog A; NKX6-1; NKX6A
    Background
    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
    • https://pubmed.ncbi.nlm.nih.gov/33121533/
    • https://pubmed.ncbi.nlm.nih.gov/23382704/

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