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Journal articles on the topic 'ALK2'

Author: Grafiati

Published: 3 June 2025

Last updated: 1 August 2025

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1

Ungefroren, Hendrik, Rüdiger Braun, Olha Lapshyna та ін. "Suppressive Role of ACVR1/ALK2 in Basal and TGFβ1-Induced Cell Migration in Pancreatic Ductal Adenocarcinoma Cells and Identification of a Self-Perpetuating Autoregulatory Loop Involving the Small GTPase RAC1b". Biomedicines 10, № 10 (2022): 2640. http://dx.doi.org/10.3390/biomedicines10102640.

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Pancreatic ductal adenocarcinoma (PDAC) cells are known for their high invasive/metastatic potential, which is regulated in part by the transforming growth factor β1 (TGFβ1). The involvement of at least two type I receptors, ALK5 and ALK2, that transmit downstream signals of the TGFβ via different Smad proteins, SMAD2/3 and SMAD1/5, respectively, poses the issue of their relative contribution in regulating cell motility. Real-time cell migration assays revealed that the selective inhibition of ALK2 by RNAi or dominant-negative interference with a kinase-dead mutant (ALK2-K233R) strongly enhanc

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Steinbicker, Andrea U., Claire Mayeur, Lisa K. Lohmeyer, et al. "Alk3, a BMP Type I Receptor Is Required for the Induction of Hepatic Hepcidin Gene Expression by Interleukin-6." Blood 118, no. 21 (2011): 686. http://dx.doi.org/10.1182/blood.v118.21.686.686.

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Abstract Abstract 686 Introduction: Anemia of chronic disease (ACD), the second most prevalent form of anemia, is commonly associated with chronic inflammatory, infectious, or neoplastic conditions. ACD is characterized by high hepcidin levels that decrease serum iron levels by inducing degradation of the iron exporter ferroportin. In contrast, a relative deficiency of hepcidin leads to ferroportin overexpression and iron overload. Hepcidin is transcriptionally regulated by interleukin-6 (IL-6) and bone morphogenic protein (BMP) signaling. Binding of BMP ligands to type II and type I BMP recep

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Olsen, Oddrun Elise, Hanne Hella, Samah Elsaadi, Carsten Jacobi, Erik Martinez-Hackert та Toril Holien. "Activins as Dual Specificity TGF-β Family Molecules: SMAD-Activation via Activin- and BMP-Type 1 Receptors". Biomolecules 10, № 4 (2020): 519. http://dx.doi.org/10.3390/biom10040519.

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Activins belong to the transforming growth factor (TGF)-β family of multifunctional cytokines and signal via the activin receptors ALK4 or ALK7 to activate the SMAD2/3 pathway. In some cases, activins also signal via the bone morphogenetic protein (BMP) receptor ALK2, causing activation of the SMAD1/5/8 pathway. In this study, we aimed to dissect how activin A and activin B homodimers, and activin AB and AC heterodimers activate the two main SMAD branches. We compared the activin-induced signaling dynamics of ALK4/7-SMAD2/3 and ALK2-SMAD1/5 in a multiple myeloma cell line. Signaling via the AL

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Backus, Thomas A., Natalia Medeiros, Evan Lema, Ffolliott Fisher, Jasbir Seehra, and Jennifer Lachey. "Selective Inhibition of ALK2 Signaling Suppresses Serum Hepcidin and Increases Serum Iron." Blood 136, Supplement 1 (2020): 14. http://dx.doi.org/10.1182/blood-2020-139486.

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Hepcidin is an endocrine regulator of iron metabolism that, when elevated, can decrease levels of iron available for erythropoiesis and, as a result, decrease red blood cell production. Signaling though activin-like kinase-2 (ALK2), a TGFβ type 1 receptor, has been implicated in regulation of hepcidin-mediated iron regulation and mobilization; however, to date, ALK2's specific degree of involvement has not been convincingly elucidated, mainly due to the redundant effects of the type 1 receptors ALK3 and ALK5. Activation of type 1 receptors including ALK2, ALK3, and ALK5 via ligand BMPs and co-

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Steinbicker, Andrea U., Thomas B. Bartnikas, Lisa K. Lohmeyer, et al. "Perturbation of hepcidin expression by BMP type I receptor deletion induces iron overload in mice." Blood 118, no. 15 (2011): 4224–30. http://dx.doi.org/10.1182/blood-2011-03-339952.

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Abstract Bone morphogenetic protein (BMP) signaling induces hepatic expression of the peptide hormone hepcidin. Hepcidin reduces serum iron levels by promoting degradation of the iron exporter ferroportin. A relative deficiency of hepcidin underlies the pathophysiology of many of the genetically distinct iron overload disorders, collectively termed hereditary hemochromatosis. Conversely, chronic inflammatory conditions and neoplastic diseases can induce high hepcidin levels, leading to impaired mobilization of iron stores and the anemia of chronic disease. Two BMP type I receptors, Alk2 (Acvr1

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Brederlau, A., R. Faigle, M. Elmi, et al. "The Bone Morphogenetic Protein Type Ib Receptor Is a Major Mediator of Glial Differentiation and Cell Survival in Adult Hippocampal Progenitor Cell Culture." Molecular Biology of the Cell 15, no. 8 (2004): 3863–75. http://dx.doi.org/10.1091/mbc.e03-08-0584.

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Bone morphogenetic proteins (BMPs) act as growth regulators and inducers of differentiation. They transduce their signal via three different type I receptors, termed activin receptor-like kinase 2 (Alk2), Alk3, or bone morphogenetic protein receptor Ia (BMPRIa) and Alk6 or BMPRIb. Little is known about functional differences between the three type I receptors. Here, we have investigated consequences of constitutively active (ca) and dominant negative (dn) type I receptor overexpression in adult-derived hippocampal progenitor cells (AHPs). The dn receptors have a nonfunctional intracellular but

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Zhang, Han, Christian Klausen, Hua Zhu, Hsun-Ming Chang, and Peter C. K. Leung. "BMP4 and BMP7 Suppress StAR and Progesterone Production via ALK3 and SMAD1/5/8-SMAD4 in Human Granulosa-Lutein Cells." Endocrinology 156, no. 11 (2015): 4269–80. http://dx.doi.org/10.1210/en.2015-1494.

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Adequate production of progesterone by the corpus luteum is critical to the successful establishment of pregnancy. In animal models, bone morphogenetic protein (BMP) 4 and BMP7 have been shown to suppress either basal or gonadotropin-induced progesterone production, depending on the species examined. However, the effects of BMP4 and BMP7 on progesterone production in human granulosa cells are unknown. In the present study, we used immortalized (SVOG) and primary human granulosa-lutein cells to investigate the effects of BMP4 and BMP7 on steroidogenic acute regulatory protein (StAR) expression

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Dulja, Alessandro, Alessia Pagani, Mariateresa Pettinato, Antonella Nai, Clara Camaschella, and Laura Silvestri. "The Immunophilin FKBP12 Inhibits Hepcidin By Modulating BMP Type I-Type II Receptors Interaction and Ligand Responsiveness." Blood 134, Supplement_1 (2019): 430. http://dx.doi.org/10.1182/blood-2019-130058.

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Introduction The liver hormone hepcidin is the master regulator of iron metabolism that modulates iron release into the circulation by binding and blocking the iron exporter ferroportin (Nemeth et al., 2004). Hepcidin expression is under the control of the BMP-SMAD pathway (Babitt et al., 2006), whose activation requires the formation of a hexameric complex composed of a dimer of BMP receptors type I (BMPR-Is), a dimer of BMPR type II (BMPR-IIs) and dimeric ligands. ALK2 and ALK3, as BMPR-Is (Steinbiecker et al., 2011), BMPR2 and ACVR2A, as BMPR-IIs (Mayeur et al., 2014), and BMP2 (Koch et al,

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Pagani, Alessia, Mariateresa Pettinato, Alessandro Dulja, et al. "Dissecting the Mechanisms of Hepcidin and BMP-SMAD Pathway Regulation By FKBP12." Blood 138, Supplement 1 (2021): 2008. http://dx.doi.org/10.1182/blood-2021-152172.

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Abstract The BMP-SMAD pathway is activated when a dimeric ligand (BMP) interacts with a dimeric serine threonine kinase receptor (BMPRII) and triggers the activation of a dimeric BMP type I receptor (BMPRI). Catalytically active BMPRIs phosphorylate SMAD1/5/8 that, upon SMAD4 binding, translocate to the nucleus to regulate the expression of BMP target genes, including hepcidin. Hepcidin is the main regulator of iron homeostasis that controls body iron levels by binding and blocking the sole iron exporter ferroportin. In agreement, hepcidin expression is homeostatically activated by serum and l

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Chen, Yaoyu, Matthew C. Stubbs, Michelle Pusey, et al. "Characterization of INCB00928, a Potent and Selective ALK2 Inhibitor for the Treatment of Anemia." Blood 136, Supplement 1 (2020): 52. http://dx.doi.org/10.1182/blood-2020-136138.

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A significant population of patients with myelofibrosis (MF) develop anemia and either require red blood cell (RBC) transfusions or have an inadequate response to the currently available therapies and become transfusion-dependent. In patients with MF, elevated levels of serum hepcidin, a key iron regulatory hormone, is associated with increased dependence on RBC transfusions and reduced overall survival. Elevated hepcidin expression has also been observed to cause severe functional iron deficiency anemia and is central to the pathophysiology of anemia of chronic disease. Thus, to ensure proper

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Xia, Yin, Jodie L. Babitt, Yisrael Sidis, Raymond T. Chung, and Herbert Y. Lin. "Hemojuvelin regulates hepcidin expression via a selective subset of BMP ligands and receptors independently of neogenin." Blood 111, no. 10 (2008): 5195–204. http://dx.doi.org/10.1182/blood-2007-09-111567.

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Abstract Hemojuvelin (HJV) is a coreceptor for bone morphogenetic protein (BMP) signaling that regulates hepcidin expression and iron metabolism. However, the precise combinations of BMP ligands and receptors used by HJV remain unknown. HJV has also been demonstrated to bind to neogenin, but it is not known whether this interaction has a role in regulating hepcidin expression. In the present study, we show that BMP-2, BMP-4, and BMP-6 are endogenous ligands for HJV in hepatoma-derived cell lines, and that all 3 of these ligands are expressed in human liver. We demonstrate in vitro that HJV sel

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Yao, Yucheng, Medet Jumabay, Albert Ly, et al. "Crossveinless 2 regulates bone morphogenetic protein 9 in human and mouse vascular endothelium." Blood 119, no. 21 (2012): 5037–47. http://dx.doi.org/10.1182/blood-2011-10-385906.

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Abstract The importance of morphogenetic proteins (BMPs) and their antagonists in vascular development is increasingly being recognized. BMP-4 is essential for angiogenesis and is antagonized by matrix Gla protein (MGP) and crossveinless 2 (CV2), both induced by the activin receptor like-kinase 1 (ALK1) when stimulated by BMP-9. In this study, however, we show that CV2 preferentially binds and inhibits BMP-9 thereby providing strong feedback inhibition for BMP-9/ALK1 signaling rather than for BMP-4/ALK2 signaling. CV2 disrupts complex formation involving ALK2, ALK1, BMP-4, and BMP-9 required f

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Szilágyi, Szabina Szófia, Wiktor Burdzinski, Jerome Jatzlau, Marcelo Ehrlich, Petra Knaus, and Yoav I. Henis. "The Activation of the Fibrodysplasia Ossificans Progressiva-Inducing ALK2-R206H Mutant Depends on the Distinct Homo-Oligomerization Patterns of ACVR2B and ACVR2A." Cells 13, no. 3 (2024): 221. http://dx.doi.org/10.3390/cells13030221.

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Mutations in activin-like kinase 2 (ALK2), e.g., ALK2-R206H, induce aberrant signaling to SMAD1/5/8, leading to Fibrodysplasia Ossificans Progressiva (FOP). In spite of extensive studies, the underlying mechanism is still unclear. Here, we quantified the homomeric and heteromeric interactions of ACVR2A, ACVR2B, ALK2-WT, and ALK2-R206H by combining IgG-mediated immobilization of one receptor with fluorescence recovery after photobleaching (FRAP) measurements on the lateral diffusion of a co-expressed receptor. ACVR2B formed stable homomeric complexes that were enhanced by Activin A (ActA), whil

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Smil, David, Héctor González-Álvarez, Deeba Ensan, et al. "Abstract A022: Discovery of conformationally constrained ALK2 inhibitors for the treatment of Diffuse Intrinsic Pontine Glioma (DIPG)." Molecular Cancer Therapeutics 23, no. 12_Supplement (2024): A022. https://doi.org/10.1158/1538-8514.cancerchem24-a022.

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Abstract Despite considerable research on new therapeutics to treat DIPG, a universally fatal grade IV pediatric CNS tumor located in the pons region of the brainstem, there has been minimal progress. Somatic missense mutations in the bone morphogenetic protein (BMP) type I receptor ACVR1 gene encoding activin receptor-like kinase-2 (ALK2) are present in approximately 33% of children with DIPG, prompting our initial efforts towards the development of M4K2009, a 3,5-diphenylpyridine ALK2 inhibitor. Looking to improve potency, selectivity, and brain penetration, we subsequently designed, synthes

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Stubbs, Matthew C., Michelle Pusey, Xiaoming Wen, et al. "ALK2 and JAK2 Inhibition for Improved Treatment of Anemia in Myelofibrosis Patients: Preclinical Profile of an ALK2 Inhibitor Zilurgisertib in Combination with Ruxolitinib." Blood 142, Supplement 1 (2023): 1789. http://dx.doi.org/10.1182/blood-2023-181055.

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Introduction: Anemia is a common occurrence in patients with myelofibrosis (MF) and is associated with the need for red blood cell transfusion and poor clinical prognosis. JAK inhibitors such as ruxolitinib are used extensively to treat symptoms of MF and improve quality of life and overall survival. However, JAK inhibitors may also contribute to myelosuppression. Therapeutic interventions that allow for optimization of JAK inhibition with no concern of anemia would benefit patients with MF and potentially lower the rate of treatment discontinuation or suboptimal dosing. Recent studies have de

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Rogers, Rebecca, Yura Grabovaska, Alan Mackay, et al. "DIPG-22. A NOVEL ROLE FOR ACVR1/ALK2 IN REGULATING CHOLESTEROL BIOSYNTHESIS PROVIDES A NEW COMBINATORIAL THERAPEUTIC APPROACH FOR PATIENTS WITH DMG." Neuro-Oncology 26, Supplement_4 (2024): 0. http://dx.doi.org/10.1093/neuonc/noae064.075.

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Abstract BACKGROUND The discovery of somatic mutations in ACVR1, which encodes the serine/threonine kinase ALK2, in 20-25% of diffuse midline glioma H3K27-altered (DMG-H3K27) patients has led to the development of numerous chemotypes of ALK2 inhibitor (ALK2i). However, in models of ACVR1-mutant DMG-H3K27 the efficacy of single-agent ALK2i’s has been modest and new combinatorial treatment approaches are desperately needed. METHODS We performed unbiased combinatorial genetic and drug screens in patient-derived ACVR1-mutant DMG-H3K27 cells in vitro, using multiple chemotypes of ALK2i. We also gen

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Visser, Jenny A., Robert Olaso, Miriam Verhoef-Post, Piet Kramer, Axel P. N. Themmen, and Holly A. Ingraham. "The Serine/Threonine Transmembrane Receptor ALK2 Mediates Müllerian Inhibiting Substance Signaling." Molecular Endocrinology 15, no. 6 (2001): 936–45. http://dx.doi.org/10.1210/mend.15.6.0645.

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Abstract Müllerian inhibiting substance (MIS or anti-Müllerian hormone) is a member of the transforming growth factor-β family and plays a pivotal role in proper male sexual differentiation. Members of this family signal by the assembly of two related serine/threonine kinase receptors, referred to as type I or type II receptors, and downstream cytoplasmic Smad effector proteins. Although the MIS type II receptor (MISRII) has been identified, the identity of the type I receptor is unclear. Here we report that MIS activates a bone morphogenetic protein-like signaling pathway, which is solely d

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Rogers, Rebecca, Maria Tsoli, Shiva Senthil Kumar, et al. "DIPG-29. A CONNECT CONSORTIUM PRECLINICAL STUDY IDENTIFIES MEK INHIBITION AND RADIATION AS POTENTIAL COMBINATION PARTNERS FOR THE ALK2 INHIBITOR TP-0184 IN ACVR1-MUTANT DMG." Neuro-Oncology 25, Supplement_1 (2023): i19. http://dx.doi.org/10.1093/neuonc/noad073.076.

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Abstract Somatic mutations in ACVR1, which encodes the serine/threonine kinase ALK2, are found in 20-25% of DMG-H3K27 patients. Treatment of ACVR1-mutant orthotopic xenografts with multiple chemotypes of ALK2 inhibitors (ALK2i) results in extended survival in vivo but, as single agents, these inhibitors are unable to achieve a complete anti-tumour response. To identify novel combination strategies alongside ALK2 inhibition, five international laboratories pooled resources to evaluate the ALK2i TP-0184 across 26 patient-derived DMG-H3K27 models in vitro, demonstrating GI50 values of ~0.5-10uM,

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Shapiro, T. N., N. A. Manucharova, and E. S. Lobakova. "Activity of alkanmonooxygenase <i>alk</i>B gene in strains of hydrocarbon-oxidizing bacteria isolated from petroleum products." Vavilov Journal of Genetics and Breeding 26, no. 6 (2022): 575–82. http://dx.doi.org/10.18699/vjgb-22-70.

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Alkanmonooxygenase enzymes AlkB and Cyp153 are responsible for the aerobic degradation of n-alkanes of petroleum and petroleum products. To prove the usage of n-alkanes from oil and petroleum products by hydrocarbon- oxidizing bacteria isolated from aviation kerosene TS-1 and automobile gasoline AI-95, the detection of the key genes alkB, Alk1, Alk2, Alk3 and Cyp153 encoding alkanmonooxygenases AlkB and Cyp153 (responsible for the oxidation of hydrocarbons with a certain chain length) was carried out. It was found that bacterial strains isolated from TS-1 jet fuel, except Deinococcus sp. Bi7,

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Shahid, Mohd, Ester Spagnolli, Laura Ernande, et al. "BMP type I receptor ALK2 is required for angiotensin II-induced cardiac hypertrophy." American Journal of Physiology-Heart and Circulatory Physiology 310, no. 8 (2016): H984—H994. http://dx.doi.org/10.1152/ajpheart.00879.2015.

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Bone morphogenetic protein (BMP) signaling contributes to the development of cardiac hypertrophy. However, the identity of the BMP type I receptor involved in cardiac hypertrophy and the underlying molecular mechanisms are poorly understood. By using quantitative PCR and immunoblotting, we demonstrated that BMP signaling increased during phenylephrine-induced hypertrophy in cultured neonatal rat cardiomyocytes (NRCs), as evidenced by increased phosphorylation of Smads 1 and 5 and induction of Id1 gene expression. Inhibition of BMP signaling with LDN193189 or noggin, and silencing of Smad 1 or

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othman, Rozhan. "INVESTIGATION OF MUTATION IN ALK2 GENE IN CARDIAC ATRIOVENTRICULAR SEPTAL DEFECT PATIENTS." Journal of Sulaimani Medical College 14, no. 1 (2024): 89–98. https://doi.org/10.17656/jsmc.10454.

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Background Activin Receptor-like Kinase 2 (ALK2) is identifi ed as a bone morphogenetic protein (BMP) type I receptor. Experimental inductions have reported that a n atrioventricular septal defect (AVSD) is caused by a mutation in ALK2 in zebrafi sh. ALK2 is one of the most infl uential factors in heart development, and mutations in this gene have been reported to be related to AVSD. Objectives Investigate the known mutation at Exon 9 of the ALK2 gene and the unknown mutation in the ALK2 gene. Defi ne if these mutations were inherited from parents or not. Investigate the regulation of the ALK2

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Renlund, Nina, Francis H. O’Neill, LiHua Zhang, Yisrael Sidis, and Jose Teixeira. "Activin receptor-like kinase-2 inhibits activin signaling by blocking the binding of activin to its type II receptor." Journal of Endocrinology 195, no. 1 (2007): 95–103. http://dx.doi.org/10.1677/joe-07-0281.

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Activin receptor-like kinase-2 (Alk2) has been shown to be a promiscuous type I receptor for the transforming growth factor β (TGFβ) family of growth and differentiation factors, such as activin, bone morphogenetic proteins, and Müllerian inhibiting substance (MIS). We have studied the putative role of Alk2 in activin signaling using MA-10 cells, a mouse transformed Leydig cell line, in which endogenous expression of cytochrome P450 c17 hydroxylase/C17–20 lyase mRNA is inhibited by both MIS and activin A. Overexpression of Alk2 in MA-10 cells inhibited the activation of the activin-responsive

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Katagiri, Takenobu, Sho Tsukamoto, and Mai Kuratani. "Accumulated Knowledge of Activin Receptor-Like Kinase 2 (ALK2)/Activin A Receptor, Type 1 (ACVR1) as a Target for Human Disorders." Biomedicines 9, no. 7 (2021): 736. http://dx.doi.org/10.3390/biomedicines9070736.

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Activin receptor-like kinase 2 (ALK2), also known as Activin A receptor type 1 (ACVR1), is a transmembrane kinase receptor for members of the transforming growth factor-β family. Wild-type ALK2/ACVR1 transduces osteogenic signaling in response to ligand binding. Fifteen years ago, a gain-of-function mutation in the ALK2/ACVR1 gene was detected in patients with the genetic disorder fibro-dysplasia ossificans progressiva, which is characterized by heterotopic ossification in soft tissues. Additional disorders, such as diffuse intrinsic pontin glioma, diffuse idiopathic skeletal hyperostosis, pri

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Fujimoto, Mai, Satoshi Ohte, Kenji Osawa, et al. "Mutant Activin-Like Kinase 2 in Fibrodysplasia Ossificans Progressiva are Activated via T203 by BMP Type II Receptors." Molecular Endocrinology 29, no. 1 (2015): 140–52. http://dx.doi.org/10.1210/me.2014-1301.

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Abstract Fibrodysplasia ossificans progressiva (FOP) is a genetic disorder characterized by progressive heterotopic ossification in soft tissues, such as the skeletal muscles. FOP has been shown to be caused by gain-of-function mutations in activin receptor-like kinase (ALK)-2, which is a type I receptor for bone morphogenetic proteins (BMPs). In the present study, we examined the molecular mechanisms that underlie the activation of intracellular signaling by mutant ALK2. Mutant ALK2 from FOP patients enhanced the activation of intracellular signaling by type II BMP receptors, such as BMPR-II

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Ramsdell, A. F., and H. J. Yost. "Cardiac looping and the vertebrate left-right axis: antagonism of left-sided Vg1 activity by a right-sided ALK2-dependent BMP pathway." Development 126, no. 23 (1999): 5195–205. http://dx.doi.org/10.1242/dev.126.23.5195.

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The rightward looping of the primary heart tube is dependent upon upstream patterning events that establish the vertebrate left-right axis. In Xenopus, a left-sided Vg1 signaling pathway has been implicated in instructing cells to adopt a ‘left-sided identity’; however, it is not known whether ‘right-sided identity’ is acquired by a default pathway or by antagonism of Vg1 signaling. Here, we propose that an antagonistic, BMP/ALK2/Smad-mediated signaling pathway is active on the right side of the Xenopus embryo. Truncated ALK2 receptor expression on the right side of the blastula elicits heart

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Basavaraja, Raghavendra, Senasige Thilina Madusanka, Ketan Shrestha, Emilia Przygrodzka, Monika Marzena Kaczmarek, and Rina Meidan. "Pentraxin-3 mediates prosurvival actions of interferon tau in bovine luteinized granulosa cells." Reproduction 160, no. 4 (2020): 603–12. http://dx.doi.org/10.1530/rep-20-0200.

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Pentraxin 3 (PTX3), a multimeric glycoprotein, is implicated in various biological functions. PTX3 was shown to be elevated in the corpus luteum (CL) of early pregnant ewes; however, its role in sheep or other ruminants’ CL during this reproductive stage or how it is regulated remain unknown. Here we explored the role of PTX3 and its relationship with interferon-tau (IFNT; the pregnancy recognition signaling molecule during early pregnancy in domestic ruminants) in bovine luteinized granulosa cells (LGCs). IFNT robustly elevated PTX3 expression in bovine LGCs, and significantly stimulated its

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Verma, Amit, Andrew M. Brunner, Gregory Pennock, et al. "Phase 1/2 Study of Oral TP-0184 for the Treatment of Anemia in Adults with Low- or Intermediate-Risk Myelodysplastic Syndromes." Blood 138, Supplement 1 (2021): 1534. http://dx.doi.org/10.1182/blood-2021-147594.

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Abstract Patients with anemia due to lower-risk myelodysplastic syndromes (MDS) have limited treatment options. The transforming growth factor β (TGF-β) pathway has been implicated in contributing to ineffective hematopoiesis in patients with MDS. Members of the TGF-β superfamily include activin receptor-like kinase 2 (ALK2) and ALK5. ALK2 signaling plays a key role in modulating hepcidin, an important regulator of iron homeostasis (and thus erythropoiesis). Increased levels of hepcidin have been linked to anemia in patients with chronic inflammation and cancer, including multiple myeloma (Mae

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Ventura, Francesc, Eleanor Williams, Makoto Ikeya, et al. "Challenges and Opportunities for Drug Repositioning in Fibrodysplasia Ossificans Progressiva." Biomedicines 9, no. 2 (2021): 213. http://dx.doi.org/10.3390/biomedicines9020213.

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Fibrodysplasia ossificans progressiva (FOP) is an ultrarare congenital disease that progresses through intermittent episodes of bone formation at ectopic sites. FOP patients carry heterozygous gene point mutations in activin A receptor type I ACVR1, encoding the bone morphogenetic protein (BMP) type I serine/threonine kinase receptor ALK2, termed activin receptor-like kinase (ALK)2. The mutant ALK2 displays neofunctional responses to activin, a closely related BMP cytokine that normally inhibits regular bone formation. Moreover, the mutant ALK2 becomes hypersensitive to BMPs. Both these activi

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Kruithof-de Julio, Marianna, Letizia Astrologo, Eugenio Zoni, et al. "Effects of ALK1Fc treatment on prostate cancer cells interacting with bone and bone cells in bone metastasis models." Journal of Clinical Oncology 35, no. 15_suppl (2017): e16576-e16576. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.e16576.

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e16576 Background: Prostate cancer is the second most common cancer in men worldwide. Lethality is normally associated with the consequences of metastasis rather than the primary tumor. In particular, bone is the most frequent site of metastasis and once prostate tumor cells are engrafted in the skeleton, curative therapy is no longer possible. Bone morphogenetic proteins (BMPs) play a critical role in bone physiology and pathology. However, little is known about the role of BMP9 and its signaling receptors, ALK1 and ALK2, in prostate cancer and bone metastasis. In this context, we investigate

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Silvestri, Laura, Alessia Pagani, Antonella Nai, and Clara Camaschella. "Novel Insights Into Systemic Iron Regulation." Blood 132, Supplement 1 (2018): SCI—1—SCI—1. http://dx.doi.org/10.1182/blood-2018-99-109518.

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Abstract Iron, an essential element in mammals, is absorbed by duodenal enterocytes, enters the circulation through the iron exporter ferroportin, (FPN), circulates bound to transferrin and is uptaken through Transferrin Receptor 1. If in excess, iron is stored in macrophages and hepatocytes and released when needed. To maintain systemic iron homeostasis and to avoid the formation of "non transferrin bound iron" (NTBI), a highly reactive form which causes organ damage, the liver synthetizes hepcidin that, binding FPN, blocks iron export to the circulation. Hepcidin integrates signals from body

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Colucci, Silvia, Alessia Pagani, Mariateresa Pettinato, et al. "The immunophilin FKBP12 inhibits hepcidin expression by binding the BMP type I receptor ALK2 in hepatocytes." Blood 130, no. 19 (2017): 2111–20. http://dx.doi.org/10.1182/blood-2017-04-780692.

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Key Points FKBP12 suppresses hepcidin by interaction with the BMP receptor ALK2. Disruption of FKBP12–ALK2 interaction increases hepcidin and renders the receptor responsive to the inflammatory ligand Activin A.

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Wu, Xiufeng, Ningning Zhang, and Mary M. Lee. "Müllerian Inhibiting Substance Recruits ALK3 to Regulate Leydig Cell Differentiation." Endocrinology 153, no. 10 (2012): 4929–37. http://dx.doi.org/10.1210/en.2012-1168.

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Abstract Müllerian inhibiting substance (MIS) not only induces Müllerian duct regression during male sexual differentiation but also modulates Leydig cell steroidogenic capacity and differentiation. MIS actions are mediated through a complex of homologous receptors: a type II ligand-binding receptor [MIS type II receptor (MISRII)] and a tissue-specific type I receptor that initiates downstream signaling. The putative MIS type I receptors responsible for Müllerian duct regression are activin A type II receptor, type I [Acvr1/activin receptor-like kinase 2 (ALK2)], ALK3, and ALK6, but the one re

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Rogers, Rebecca, Diana Carvalho, Yura Grabovska, et al. "DIPG-40. Combined pharmacological and genetic screening to identify dependencies and combinations in ACVR1-mutant diffuse midline glioma." Neuro-Oncology 24, Supplement_1 (2022): i27. http://dx.doi.org/10.1093/neuonc/noac079.097.

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Abstract Somatic mutations in ACVR1, which encodes the serine/threonine kinase ALK2, are found in 20-25% of DMG-H3K27 patients. Treatment of ACVR1-mutant patient-derived models with multiple chemotypes of ALK2 inhibitors (ALK2i) results in reduced cell viability in vitro and extended survival in orthotopic xenografts in vivo but, as single agents, these inhibitors were unable to achieve a complete anti-tumour response. Recently we reported that combinatorial treatment of ACVR1-mutant DIPG cells with vandetanib (RTK inhibitor) and everolimus (mTOR/ABC transporter inhibitor) was synergistic both

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Rogers, Rebecca, Diana Carvalho, Yura Grabovska, et al. "EXTH-41. COMBINED PHARMACOLOGICAL AND GENETIC SCREENING TO IDENTIFY DEPENDENCIES AND COMBINATIONS IN ACVR1-MUTANT DIFFUSE MIDLINE GLIOMA." Neuro-Oncology 24, Supplement_7 (2022): vii218. http://dx.doi.org/10.1093/neuonc/noac209.839.

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Abstract Somatic mutations in ACVR1, which encodes the serine/threonine kinase ALK2, are found in 20-25% of DMG-H3K27 patients. Treatment of ACVR1-mutant patient-derived models with multiple chemotypes of ALK2 inhibitors (ALK2i) results in reduced cell viability in vitro and extended survival in orthotopic xenografts in vivo but, as single agents, these inhibitors were unable to achieve a complete anti-tumour response. Recently we reported that combinatorial treatment of ACVR1-mutant DIPG cells with vandetanib (RTK inhibitor) and everolimus (mTOR/ABC transporter inhibitor) was synergistic both

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Peng, Wanli, Xiuli Wang, Qinchen Liu, et al. "The GntR/VanR transcription regulator AlkR represses AlkB2 monooxygenase expression and regulates n‐alkane degradation in Pseudomonas aeruginosa SJTD‐1." mLife 4, no. 2 (2025): 126–42. https://doi.org/10.1002/mlf2.70004.

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AbstractTransmembrane alkane monooxygenase (AlkB)‐type monooxygenases, especially AlkB2 monooxygenases, are crucial for aerobic degradation of the medium‐to‐long‐chain n‐alkanes in hydrocarbon‐utilizing microorganisms. In this study, we identified a GntR/VanR transcription regulator AlkR of Pseudomonas aeruginosa SJTD‐1 involved in the negative regulation of AlkB2 and deciphered its nature of DNA binding and ligand release. The deletion of alkR enhanced the transcription levels of the alkB2 gene and the utilization efficiency of the medium‐to‐long‐chain n‐alkanes by strain SJTD‐1. The dimer of

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Traeger, Lisa, Inka Gallitz, Rohit Sekhri, et al. "ALK3 undergoes ligand-independent homodimerization and BMP-induced heterodimerization with ALK2." Free Radical Biology and Medicine 129 (December 2018): 127–37. http://dx.doi.org/10.1016/j.freeradbiomed.2018.09.021.

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Daly, Amanda C., Rebecca A. Randall та Caroline S. Hill. "Transforming Growth Factor β-Induced Smad1/5 Phosphorylation in Epithelial Cells Is Mediated by Novel Receptor Complexes and Is Essential for Anchorage-Independent Growth". Molecular and Cellular Biology 28, № 22 (2008): 6889–902. http://dx.doi.org/10.1128/mcb.01192-08.

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ABSTRACT Transforming growth factor β (TGF-β) signals predominantly through a receptor complex comprising ALK5 and TβRII to activate receptor-regulated Smads (R-Smads) Smad2 and Smad3. In endothelial cells, however, TGF-β can additionally activate Smad1 and Smad5. Here, we report that TGF-β also strongly induces phosphorylation of Smad1/5 in many different normal epithelial cells, epithelium-derived tumor cells, and fibroblasts. We demonstrate that TβRII and ALK5, as well as ALK2 and/or ALK3, are required for TGF-β-induced Smad1/5 phosphorylation. We show that the simultaneous activation of th

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De Rycke, Ophélie, Thomas Walter, Marine Perrier, et al. "Alkylating agent rechallenge in metastatic pancreatic neuroendocrine tumors." Endocrine-Related Cancer 28, no. 7 (2021): 457–66. http://dx.doi.org/10.1530/erc-21-0034.

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A rechallenge is common after the initial efficacy of alkylating-based chemotherapy (ALK) in pancreatic neuroendocrine tumors (PanNET). High MGMT expression seems associated with a lower response to ALK. We aimed to evaluate the efficacy and toxicity of ALK rechallenge in PanNET, and to assess the evolution of MGMT expression under ALK. All consecutive patients with advanced PanNETs who received initial ALK (achieving tumor control) followed by a pause of > 3 months, then an ALK rechallenge (ALK2) upon progression were retrospectively studied (cohort A). The primary endpoint was progression

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Shao, Esther S., Laura Lin, Yucheng Yao, and Kristina I. Boström. "Expression of vascular endothelial growth factor is coordinately regulated by the activin-like kinase receptors 1 and 5 in endothelial cells." Blood 114, no. 10 (2009): 2197–206. http://dx.doi.org/10.1182/blood-2009-01-199166.

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Abstract Expression of vascular endothelial growth factor (VEGF) is tightly regulated to achieve normal angiogenesis. The objective was to examine regulation of VEGF by the activin-like kinase receptors (ALKs) ALK1 and ALK5. Transforming growth factor β1 (TGFβ1) and bone morphogenetic protein-9 (BMP-9) enhanced and suppressed VEGF expression, respectively, in aortic endothelial cells, as determined by real-time polymerase chain reaction, immunoblotting, cell proliferation, and tube formation. The use of small interfering RNA revealed that TGFβ1 stimulated VEGF expression by activating ALK5, TG

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Medeiros, Natalia, Thomas A. Backus, Christopher Materna, Ffolliott Fisher, Jenn Lachey, and Jasbir Seehra. "A Monoclonal Antibody Targeting ALK2 As a Potential Therapeutic Agent for Anemia of Inflammation." Blood 138, Supplement 1 (2021): 2007. http://dx.doi.org/10.1182/blood-2021-153160.

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Abstract Background: Iron homeostasis is primarily regulated by hepcidin, a hormone predominantly expressed in the liver. Hepcidin activates the degradation of the transmembrane iron exporter ferroportin, thereby downregulating the release of iron from cells. Hepcidin expression is, at least partly, regulated in response to signaling of the type I TGF-β receptor ALK2, via SMAD2/3 phosphorylation. IL-6, which is commonly elevated in chronic kidney disease (CKD) and other inflammatory conditions, upregulates hepcidin expression and reduces serum iron bioavailability. As a result, chronic inflamm

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Marín, Mercedes M., Luis Yuste, and Fernando Rojo. "Differential Expression of the Components of the Two Alkane Hydroxylases from Pseudomonas aeruginosa." Journal of Bacteriology 185, no. 10 (2003): 3232–37. http://dx.doi.org/10.1128/jb.185.10.3232-3237.2003.

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ABSTRACT Oxidation of n-alkanes in bacteria is normally initiated by an enzyme system formed by a membrane-bound alkane hydroxylase and two soluble proteins, rubredoxin and rubredoxin reductase. Pseudomonas aeruginosa strains PAO1 and RR1 contain genes encoding two alkane hydroxylases (alkB1 and alkB2), two rubredoxins (alkG1 and alkG2), and a rubredoxin reductase (alkT). We have localized the promoters for these genes and analyzed their expression under different conditions. The alkB1 and alkB2 genes were preferentially expressed at different moments of the growth phase; expression of alkB2 w

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Williams, Eleanor, Elise Riesebos, Georgina Kerr, and Alex N. Bullock. "ALK2 Receptor Kinase Association with FKBP12.6 Is Structurally Conserved with the ALK2-FKBP12 Complex." Biomedicines 9, no. 2 (2021): 129. http://dx.doi.org/10.3390/biomedicines9020129.

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The immunophilin FKBP12 is a known inhibitor of type I BMP and TGF-β receptors that competes for binding with their substrate SMADs. FKBP12 and the close paralog FKBP12.6 additionally assemble with ryanodine receptors to control Ca2+ release. Binding of FKBP12.6 to BMP/TGF-β receptors has yet to be investigated, but appears plausible given its high sequence similarity to FKBP12. Here, we found that FKBP12.6 can assemble with BMP and TGF-β-family type I receptors, but not with type II receptors. Cellular immunoprecipitation confirmed similar binding of FKBP12 and FKBP12.6 to the BMP receptor AL

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Tyagi, Anudishi, Stanley Ly, Bin Yuan, et al. "TP-0184, a Novel FLT3-ALK2 Dual Inhibitor, Targets Amino Acid Transport and Biosynthesis in AML Cells and Sensitizes AML Cells to Chemotherapy and BCL2 Inhibition." Blood 138, Supplement 1 (2021): 376. http://dx.doi.org/10.1182/blood-2021-151251.

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Abstract Background FMS-like tyrosine kinase 3 (FLT3), a transmembrane receptor tyrosine kinase that is frequently mutated in AML, is associated with poor prognosis. Inhibitors of FLT3 internal tandem duplication (ITD) mutants and wild-type (WT) FLT3 have been studied, but their clinical usefulness is limited owing to treatment resistance. However, the molecular factors contributing to this resistance are unknown. We reported that AML cells induce osteogenic differentiation of bone marrow-derived mesenchymal stromal cells through the bone morphogenetic protein (BMP)-mediated signaling pathway,

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WANG, SHI-NONG, JANINE LAPAGE, and RAIMUND HIRSCHBERG. "Loss of Tubular Bone Morphogenetic Protein—7 in Diabetic Nephropathy." Journal of the American Society of Nephrology 12, no. 11 (2001): 2392–99. http://dx.doi.org/10.1681/asn.v12112392.

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Abstract. Bone morphogenetic protein—7 (BMP7), a member of the transforming growth factor—β (TGF—β) superfamily of cytokines, is highly expressed in renal tubules and generally promotes maintenance of epithelial phenotype. It was examined whether, during the evolution of experimental diabetic nephropathy, the renal expression of BMP7 and BMP7 receptors declines, and the hypothesis that loss of BMP7 activity is profibrogenic in proximal tubular cells was tested. Moreover,in vitrostudies in cultured proximal tubular cells were performed to examine putative mechanisms that cause these changes. At

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Xu, Annie. "Fibrodysplasia Ossificans Progressiva: Molecular Mechanism, Drug Development and Current Clinical Trials." International Journal of Biomedical Science 19, no. 1 (2023): 18–25. http://dx.doi.org/10.59566/ijbs.2023.19018.

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Fibrodysplasia ossificans progressiva (FOP) is a rare genetic human disease characterized by abnormal bone formation in muscle and soft tissues of the patient, due to dysregulated activity of the bone morphogenetic protein (BMP) signaling. Activin A receptor type I (ACVR1), also known as Activin-like kinase 2 (ALK2), is a key BMP type I receptor for the normal BMP signaling transduction. The heterozygous missense mutations in ALK2 are the root cause of FOP, and ALK2R206H accounts for approximately 97% of all FOP cases. Cumulative studies have shown that Activin A, which normally activates TGF

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Rooney, Lisa, and Chris Jones. "Recent Advances in ALK2 Inhibitors." ACS Omega 6, no. 32 (2021): 20729–34. http://dx.doi.org/10.1021/acsomega.1c02983.

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Wang, Ying, Catherine C. Ho, EunJin Bang, et al. "Bone Morphogenetic Protein 2 Stimulates Noncanonical SMAD2/3 Signaling via the BMP Type 1A Receptor in Gonadotrope-Like Cells: Implications for FSH Synthesis." Endocrinology 155, no. 5 (2014): 1970–81. http://dx.doi.org/10.1210/en.2013-1741.

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FSH is an essential regulator of mammalian reproduction. Its synthesis by pituitary gonadotrope cells is regulated by multiple endocrine and paracrine factors, including TGFβ superfamily ligands, such as the activins and inhibins. Activins stimulate FSH synthesis via transcriptional regulation of its β-subunit gene (Fshb). More recently, bone morphogenetic proteins (BMPs) were shown to stimulate murine Fshb transcription alone and in synergy with activins. BMP2 signals via its canonical type I receptor, BMPR1A (or activin receptor-like kinase 3 [ALK3]), and SMAD1 and SMAD5 to stimulate transcr

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Witten, Michael R., Liangxing Wu, Cheng-Tsung Lai, et al. "Inhibition of ALK2 with bicyclic pyridyllactams." Bioorganic & Medicinal Chemistry Letters 55 (January 2022): 128452. http://dx.doi.org/10.1016/j.bmcl.2021.128452.

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Lee, Heon-Woo, Diana C. Chong, Roxana Ola, et al. "Alk2/ACVR1 and Alk3/BMPR1A Provide Essential Function for Bone Morphogenetic Protein–Induced Retinal Angiogenesis." Arteriosclerosis, Thrombosis, and Vascular Biology 37, no. 4 (2017): 657–63. http://dx.doi.org/10.1161/atvbaha.116.308422.

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Nespoli, Alessandro, Raffaella Vercillo, Lisa di Nola, et al. "Alk1 and Alk2 are Two New Cell Cycle-Regulated Haspin-Like Proteins in Budding Yeast." Cell Cycle 5, no. 13 (2006): 1464–71. http://dx.doi.org/10.4161/cc.5.13.2914.

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