MW 570.7 Da. Potent and selective inhibitor of the Parkinson's disease kinase LRRK2. Benzodiazepine based derivative. Inhibits both G2019S mutant and wild-type LRRK2 kinase activity (IC50 values are 6 and 13 nM respectively). Causes dephosphorylation, ubiquitination and degradation of LRRK2. Inhibits IFN-γ-induced monocyte maturation in vitro.
AURA17, Beta-interferon, Dardarin, Fibroblast interferon, Hypothetical protein FLJ35932, IFB, IFF, IFN-beta, IFNB 1, IFNB_HUMAN, Interferon beta, Interferon beta 1 fibroblast, Interferon beta precursor, LRRK2_HUMAN, Leucine rich repeat kinase 2, Leucine-rich repeat serine/threonine-protein kinase 2, MGC96956, PARK 8, RIPK7, ROCO 2, STK33_HUMAN, Serine threonine kinase 33, Serine/threonine kinase 33, Serine/threonine-protein kinase 33, augmented in rheumatoid arthritis 17, leucine rich repeat serine threonine protein kinase 2
MW 570.7 Da. Potent and selective inhibitor of the Parkinson's disease kinase LRRK2. Benzodiazepine based derivative. Inhibits both G2019S mutant and wild-type LRRK2 kinase activity (IC50 values are 6 and 13 nM respectively). Causes dephosphorylation, ubiquitination and degradation of LRRK2. Inhibits IFN-γ-induced monocyte maturation in vitro.
Soluble in DMSO.
Soluble in ethanol up to 100mM.
Potent and selective inhibitor of the Parkinson's disease kinase LRRK2. Benzodiazepine based derivative. Inhibits both G2019S mutant and wild-type LRRK2 kinase activity (IC50 values are 6 and 13 nM respectively). Causes dephosphorylation, ubiquitination and degradation of LRRK2. Inhibits IFN-γ-induced monocyte maturation in vitro.
Interferon beta also known as IFN-β is a cytokine with a molecular mass of approximately 20 kDa. It belongs to the Type I interferon family. IFN-β gets produced mainly by fibroblasts and some types of epithelial cells. Its expression usually occurs in response to viral infections. Besides immune modulation it affects cell signaling through the JAK-STAT pathway. In addition STK33 and LRRK2 act as kinases with STK33 being expressed in various tissues and associated with cancer cell survival while LRRK2 is largely expressed in the brain and connected with neuronal function and inflammation. LRRK2-in-1 is a known LRRK2 inhibitor.
Interferon beta participates in antiviral defense by inducing the expression of interferon-stimulated genes. It does not form part of a complex but interacts directly with its receptor IFNAR. In contrast STK33 and LRRK2 function as part of larger kinase complexes. STK33's role remains less clear often linked to serine/threonine phosphorylation involved in survival pathways. LRRK2 frequently referred to in literature for its full name leucine-rich repeat kinase 2 heavily contributes to autophagy and apoptosis regulatory processes.
Interferon beta mainly involves itself in the JAK-STAT signaling pathway that regulates immune response. This pathway influences not only immune cell activation but also gene expression critical for viral defense. STK33 associates with pathways relevant to cell growth intersecting with kinases like mTOR. LRRK2 takes part in the MAPK/ERK pathway related to inflammatory responses alongside proteins such as Rab GTPases. LRRK2 inhibitors demonstrate potential in modulating these pathways for therapeutic advances.
Interferon beta finds applications in multiple sclerosis treatment due to its ability to modulate immune responses and reduce inflammation. STK33's role in cancer makes it a potential therapeutic target with ongoing research examining its involvement in tumor progression. LRRK2 connects to Parkinson's disease through mutations that influence its kinase activity affecting neuronal survival. The modulation of LRRK2 inhibitors shows promise in ameliorating neurologic symptoms with studies also linking LRRK2 to alpha-synuclein a protein implicated in Parkinson's disease.
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