MW 710.9 Da, Purity >98%. Potent HIF signaling inhibitor. Reduces CA9 and VEGF expression in hypoxic cells (IC50 = 10 nM, secreted VEGF, Hep38 cells). Shows antibacterial and antifungal effects. Shows antitumor effects in vivo. .
H3-K9-HMTase 1, Histone H3-K9 methyltransferase1, Histone lysine N methyltransferase, H3 lysine 9 specific 1, Histone-lysine N-methyltransferase SUV39H1, KMT1 A, Lysine N-methyltransferase 1A, MG44, Position-effect variegation 3-9 homolog, SUV39 H1, SUV39H, SUV91_HUMAN, Su(var)3-9 homolog 1, Suppressor of variegation 3 9 homolog 1 (Drosophila), Suppressor of variegation 3-9 homolog 1, mIS6
MW 710.9 Da, Purity >98%. Potent HIF signaling inhibitor. Reduces CA9 and VEGF expression in hypoxic cells (IC50 = 10 nM, secreted VEGF, Hep38 cells). Shows antibacterial and antifungal effects. Shows antitumor effects in vivo. .
Soluble in DMSO.
Potent HIF signaling inhibitor. Reduces CA9 and VEGF expression in hypoxic cells (IC50 = 10 nM, secreted VEGF, Hep38 cells). Shows antibacterial and antifungal effects. Shows antitumor effects in vivo.
KMT1A also known as SUV39H1 is a well-studied histone methyltransferase responsible for trimethylating histone H3 at lysine 9 (H3K9me3) an important marker for heterochromatin formation. This enzyme plays a critical role in chromatin organization and gene regulation. KMT1A has a molecular weight of approximately 48 kDa. Researchers have observed its expression across a range of tissues including the brain heart and muscle which suggests its importance in various physiological processes.
KMT1A functions as part of a Suv39H1/HP1 complex that maintains the integrity of pericentric heterochromatin essential for chromosome stability during cell division. Its influence extends over the transcriptional silencing of specific genes by modifying chromatin structure to a closed state. KMT1A also collaborates with other proteins like HP1 to silence repetitive elements and prevent genomic instability which is often important for safeguarding genomic fidelity in cells.
Researchers identify KMT1A as a significant player in the regulation of epigenetic pathways particularly the histone methylation process. It interacts closely with other histone methyltransferases and demethylases contributing to a dynamic epigenetic landscape that controls gene expression. Additionally KMT1A is involved in the DNA damage response pathway in collaboration with proteins like ATM which coordinates repair mechanisms to maintain genetic stability and respond to cellular stress.
Researchers have linked KMT1A with cancer and neurodegenerative diseases such as Huntington’s disease. Abnormal expression or function of KMT1A can lead to disrupted heterochromatin structure and uncontrolled gene expression which contributes to tumorigenesis. Furthermore in the context of neurodegenerative conditions interactions with proteins such as HTT can exacerbate neuronal damage and cell death. Studying these associations provides insights into potential therapeutic targets for managing such diseases.
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2D chemical structure image of ab144222, Chetomin, HIF signaling inhibitor
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