{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMyosin light chain 9 (MYL9) is a regulatory component of the contractile apparatus that plays a pivotal role in smooth muscle contraction and cellular cytokinesis. Mechanistically, MYL9 phosphorylation is a crucial regulatory step in myosin-driven contraction, as illustrated by studies showing that its loss is associated with disorders of smooth muscle function such as megacystis‐microcolon‐intestinal hypoperistalsis syndrome, where a homozygous deletion of MYL9 likely disrupts normal smooth muscle contractility. In addition, recruitment of MYL9 to the cleavage furrow during telophase, through interactions mediated by proteins such as Arv1, is essential for proper cell division and cytokinesis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": ""}, {"type": "p", "children": [{"type": "t", "text": "\nIn the context of cancer, aberrant expression and mis-regulation of MYL9 have been implicated in tumor progression, metastasis, and altered cell motility. Several studies have observed that MYL9 expression is frequently downregulated in malignancies such as non‐small cell lung cancer and prostate cancer, with reduced levels correlating with advanced pathological stage, metastasis, and poorer clinical outcomes. Moreover, MYL9 is transcriptionally regulated by factors such as the MRTF-A/SMYD3 complex—promoting migration in breast cancer—and its ability to bind to key mediators like Yes-associated protein 1 (YAP1) has been shown to drive cell proliferation, invasion, migration, and angiogenesis in colorectal cancer. Recent reviews further support a role for MYL9 in immune infiltration and tumor invasiveness."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "3", "end_ref": "9"}]}, {"type": "t", "text": ""}, {"type": "p", "children": [{"type": "t", "text": "\nMYL9 also has important roles in hematopoietic and immune cell functions. In megakaryopoiesis, the MAL/SRF transcriptional complex directly regulates MYL9 expression, which is vital for proplatelet formation and proper platelet function. In inflammatory settings, MYL9 released from activated platelets forms “MYL9 nets” that facilitate the recruitment and retention of CD69‐expressing effector cells, contributing to the pathogenesis of conditions such as Kawasaki disease and inflammatory bowel disease. In T cells, MYL9 expression is linked to enhanced surface CD3 presentation, while its different isoforms have been characterized in hematopoietic lineages. Moreover, remodeling processes in endometrial stromal cells mediated by the RhoA/ROCK1/MYL9 pathway further underscore the versatility of MYL9 in regulating cytoskeletal dynamics and cell migration."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "10", "end_ref": "16"}]}]}]}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Hilde Sundvold, Vibeke Sundvold-Gjerstad, Helle Malerød-Fjeld, et al. 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