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Artículos de revistas sobre el tema "LNK"

Autor: Grafiati

Publicado: 10 de marzo de 2023

Última modificación: 31 de julio de 2025

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1

koren-Michowitz, Maya, Sigal Gery, Daniel Nowak, et al. "Adaptor Protein LNK Binds to and Is Phosphorylated by JAK3 and May Serve as a Scaffold for JAK3 Autophosphorylation In the Absence of An Appropriate Cytokine Receptor." Blood 116, no. 21 (2010): 2785. http://dx.doi.org/10.1182/blood.v116.21.2785.2785.

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Abstract Abstract 2785 The adaptor protein LNK has an important role during the development and maturation of cells in the hematopoietic system. LNK KO mice have an expansion of hematopoietic stem cells (HSCS) and an increase in circulating neutrophils, platelets, as well as immature B cells. On the other hand, overexpression of WT LNK under the control of a lymphocyte-specific expression vector results in an impaired expansion of lymphoid precursor cells and altered mature B cell subpopulations. Recently, LNK PH domain mutations were described in myeloproliferative neoplasms (MPN). The non-re

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2

Dou, Huijuan, Andriana Kotini, Wenli Liu, et al. "Oxidized Phospholipids Promote NETosis and Arterial Thrombosis in LNK(SH2B3) Deficiency." Circulation 144, no. 24 (2021): 1940–54. http://dx.doi.org/10.1161/circulationaha.121.056414.

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Background: LNK/SH2B3 inhibits Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling by hematopoietic cytokine receptors. Genome-wide association studies have shown association of a common single nucleotide polymorphism in LNK (R262W, T allele) with neutrophilia, thrombocytosis, and coronary artery disease. We have shown that LNK(TT ) reduces LNK function and that LNK-deficient mice display prominent platelet–neutrophil aggregates, accelerated atherosclerosis, and thrombosis. Platelet–neutrophil interactions can promote neutrophil extracellular trap (NET) formation

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3

Tabayashi, Takayuki, Sigal Gery, Maya Koren-Michowitz, and H. Phillip Koeffler. "Adaptor Protein Lnk Negatively Regulates Bcr-Abl-Induced Cell Proliferation through Inhibition of the Stat5 Signaling Pathway." Blood 116, no. 21 (2010): 3406. http://dx.doi.org/10.1182/blood.v116.21.3406.3406.

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Abstract Abstract 3406 Adaptor protein Lnk negatively regulates not only several hematopoietic cytokine receptors including MPL, EpoR and c-Kit, but also non-receptor tyrosine kinases such as JAK2 and Src. Our previous studies demonstrated that Lnk, when expressed in hematopoietic cell lines, binds and regulates the mutant proteins, JAK2V617F and MPLW515L. Recent in vivo studies have shown that Lnk has an important role in the development of myeloproliferative neoplasms. These data suggest that Lnk may have the ability to inhibit constitutively activated signaling pathways in hematopoietic mal

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4

Gery, Sigal, Saskia Gueller, Julia Sohn, Shayne Nabavinouri, Amanda Leiter, and H. Phillip Koeffler. "Adaptor Protein Lnk Negatively Regulates Mutant MPL and JAK2 Alleles Associated with Myeloproliferative Disorders." Blood 110, no. 11 (2007): 1531. http://dx.doi.org/10.1182/blood.v110.11.1531.1531.

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Abstract Activating mutations in the cytokine receptor/JAK2 signaling axis are found at high frequency in myeloproliferative disorders (MPD). Lnk, an SH2-containing adaptor protein, is a negative regulator of several hematopoietic cytokine receptors including MPL and EpoR. Here, we assessed whether Lnk can attenuate the activity of mutant MPLW515L, JAK2V617F and JAK2K539L found in MPD patients. Lnk overexpression in Ba/F3-MPLW515L cells inhibited cytokine-independent growth, while suppression of Lnk in UT7-MPLW515L cells enhanced proliferation. Lnk-mediated growth inhibition was associated wit

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5

Kiladjian, Jean-Jacques, Fanny Baran-Marszak, Christophe Desterke, et al. "Abnormal Expression and Function of the Lnk Adaptor Protein in Myeloproliferative Neoplasms (MPN)." Blood 114, no. 22 (2009): 2897. http://dx.doi.org/10.1182/blood.v114.22.2897.2897.

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Abstract Abstract 2897 Poster Board II-873 Introduction: We have shown in a deficient mouse model that the adaptor protein Lnk had an important role as negative regulator of cytokine signaling during hematopoiesis (Velazquez et al., J. Exp Med 2002). Lnk-/- animals display abnormal megakaryopoiesis sharing many features with that found in MPN patients. This phenotype is due to loss of Lnk inhibition of thrombopoietin (TPO)-mediated JAK2 activation (Tong et al., J Exp Med 2004). Recent studies have shown that Lnk, when expressed in hematopoietic cell lines, could bind and regulate two mutant pr

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6

Takaki, Satoshi, Julian D. Watts, Katherine A. Forbush, et al. "Characterization of Lnk." Journal of Biological Chemistry 272, no. 23 (1997): 14562–70. http://dx.doi.org/10.1074/jbc.272.23.14562.

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7

Eto, Koji, Hitoshi Takizawa, Satoshi Takaki, Hidekazu Nishikii, Atsushi Oda та Hiromitsu Nakauchi. "The Cytokine Signal Inhibitor Lnk Promotes αIIbβ3 Integrin Outside-In Signaling through β3 Tyrosine Phosphorylation in Platelets." Blood 110, № 11 (2007): 3651. http://dx.doi.org/10.1182/blood.v110.11.3651.3651.

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Abstract Lnk is an SH2 domain-containing adapter protein that inhibits cytokine signaling. Lnk−/− mice exhibit a marked increase in numbers of hematopoietic stem cells, megakaryocytes and platelets, presumably due to the lack of negative regulation in thrombopoietin-mediated signals by Lnk. We previously reported that Lnk might play an unanticipated role in platelet integrin αIIbβ3 outside-in signaling. Lnk−/− platelets exhibited defects in full spreading on fibrinogen, clot retraction and formation of thrombi on collagen under flow conditions while they showed normal inside-out signaling (Blo

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8

Tong, Wei, Jing Zhang, and Harvey F. Lodish. "Lnk inhibits erythropoiesis and Epo-dependent JAK2 activation and downstream signaling pathways." Blood 105, no. 12 (2005): 4604–12. http://dx.doi.org/10.1182/blood-2004-10-4093.

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Abstract Erythropoietin (Epo), along with its receptor EpoR, is the principal regulator of red cell development. Upon Epo addition, the EpoR signaling through the Janus kinase 2 (JAK2) activates multiple pathways including Stat5, phosphoinositide-3 kinase (PI-3K)/Akt, and p42/44 mitogen-activated protein kinase (MAPK). The adaptor protein Lnk is implicated in cytokine receptor signaling. Here, we showed that Lnk-deficient mice have elevated numbers of erythroid progenitors, and that splenic erythroid colony-forming unit (CFU-e) progenitors are hypersensitive to Epo. Lnk-/- mice also exhibit su

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9

de Leone, María José, Carlos Esteban Hernando, Andrés Romanowski, et al. "The LNK Gene Family: At the Crossroad between Light Signaling and the Circadian Clock." Genes 10, no. 1 (2018): 2. http://dx.doi.org/10.3390/genes10010002.

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Light signaling pathways interact with the circadian clock to help organisms synchronize physiological and developmental processes to periodic environmental cycles. The plant photoreceptors responsible for clock resetting have been characterized, but signaling components that link the photoreceptors to the clock remain to be identified. Members of the family of NIGHT LIGHT–INDUCIBLE AND CLOCK-REGULATED (LNK) genes play key roles linking light regulation of gene expression to the control of daily and seasonal rhythms in Arabidopsis thaliana. Particularly, LNK1 and LNK2 were shown to control cir

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10

Balcerek, Joanna, Jing Jiang, Alexey Bersenev, Yiwen Song, Chao Wu, and Wei Tong. "14-3-3 Regulates the Lnk/JAK2 Pathway In Hematopoietic Stem and Progenitor Cells." Blood 116, no. 21 (2010): 86. http://dx.doi.org/10.1182/blood.v116.21.86.86.

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Abstract Abstract 86 Hematopoietic stem and progenitor cell (HSPC) homeostasis is regulated by intricate signaling networks. The tyrosine kinase JAK2 plays an essential role in cytokine signaling during hematopoiesis and its dysregulation can lead to hematologic malignancies. Recently activating mutations in JAK2 were found in a large fraction of patients with myeloproliferative neoplasms (MPNs). We previously demonstrated that lymphocyte adaptor protein (Lnk) binds JAK2 and attenuates its activity, thereby limiting HSPC expansion (Bersenev et al., JCI, 2008;118:2832-2844). We further showed t

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11

Lin, De-Chen, Tong Yin, Maya Koren-Michowitz, et al. "Adaptor protein Lnk binds to and inhibits normal and leukemic FLT3." Blood 120, no. 16 (2012): 3310–17. http://dx.doi.org/10.1182/blood-2011-10-388611.

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Abstract Fms-like tyrosine kinase 3 (FLT3) is a receptor tyrosine kinase with important roles in hematopoietic progenitor cell survival and proliferation. It is mutated in approximately one-third of AML patients, mostly by internal tandem duplications (ITDs). Adaptor protein Lnk is a negative regulator of hematopoietic cytokine signaling. In the present study, we show that Lnk interacts physically with both wild-type FLT3 (FLT3-WT) and FLT3-ITD through the SH2 domains. We have identified the tyrosine residues 572, 591, and 919 of FLT3 as phosphorylation sites involved in direct binding to Lnk.

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12

Nobuhisa, Ikuo, Makiko Takizawa, Satoshi Takaki, et al. "Regulation of Hematopoietic Development in the Aorta-Gonad-Mesonephros Region Mediated by Lnk Adaptor Protein." Molecular and Cellular Biology 23, no. 23 (2003): 8486–94. http://dx.doi.org/10.1128/mcb.23.23.8486-8494.2003.

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ABSTRACT Development of hematopoietic cells in the aorta-gonad-mesonephros (AGM) region in the midgestation mouse embryo involves a multistep process, sequentially changing from endothelial cell-like cells, including hemangioblasts, into hematopoietic stem cells, progenitors, and/or lineage-committed cells. An adaptor molecule, Lnk, is known to negatively control the production of pro- and pre-B cells and hematopoietic progenitor cells in adult bone marrow. Here we show a role of Lnk in hematopoietic development in the AGM region. Lnk was predominantly expressed in the endothelial cells lining

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13

Velazquez, Laura, Alec M. Cheng, Heather E. Fleming, et al. "Cytokine Signaling and Hematopoietic Homeostasis Are Disrupted in Lnk-deficient Mice." Journal of Experimental Medicine 195, no. 12 (2002): 1599–611. http://dx.doi.org/10.1084/jem.20011883.

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The adaptor protein Lnk, and the closely related proteins APS and SH2B, form a subfamily of SH2 domain-containing proteins implicated in growth factor, cytokine, and immunoreceptor signaling. To elucidate the physiological function of Lnk, we derived Lnk-deficient mice. Lnk−/− mice are viable, but display marked changes in the hematopoietic compartment, including splenomegaly and abnormal lymphoid and myeloid homeostasis. The in vitro proliferative capacity and absolute numbers of hematopoietic progenitors from Lnk−/− mice are greatly increased, in part due to hypersensitivity to several cytok

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14

Hossain, Md Akram, Brijendra Singh, Jeremie Fages, Carlo Salas Salinas, Xiao Hua Liang, and Wei Tong. "Lnk/Sh2b3 Deficiency Increases DNA Damage Tolerance to Promote Hematopoietic Stem Cell Fitness." Blood 142, Supplement 1 (2023): 32. http://dx.doi.org/10.1182/blood-2023-190875.

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DNA repair deficiency depicted by the syndrome Fanconi Anemia (FA), results in progressive bone marrow failure (BMF), increased leukemia incidence and cancer susceptibility. Out of the 23 causative genes for FA, FANCD2 is crucial for its central role in the regulation of DNA repair and replication. The FA pathway plays an important role in maintaining hematopoietic stem and progenitor cell (HSPC) homeostasis and genome integrity. Our previous studies revealed that loss of the adaptor protein LNK (SH2B3), a negative regulator of cytokine signaling, restores hematopoietic stem cell (HSC) functio

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15

Hao, Meihua, Feng Yuan, Chenchen Jin, et al. "Overexpression of Lnk in the Ovaries Is Involved in Insulin Resistance in Women With Polycystic Ovary Syndrome." Endocrinology 157, no. 10 (2016): 3709–18. http://dx.doi.org/10.1210/en.2016-1234.

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Polycystic ovary syndrome (PCOS) progression involves abnormal insulin signaling. SH2 domain-containing adaptor protein (Lnk) may be an important regulator of the insulin signaling pathway. We investigated whether Lnk was involved in insulin resistance (IR). Thirty-seven women due to receive laparoscopic surgery from June 2011 to February 2012 were included from the gynecologic department of the Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University. Samples of polycystic and normal ovary tissues were examined by immunohistochemistry. Ovarian cell lines underwent insulin stimulation and Lnk ove

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16

Lasho, Terra, Ayalew Tefferi, Alessandro M. Vannucchi, et al. "LNK Mutation Studies In Chronic- and Blast-Phase Myeloproliferative Neoplasms and JAK2 Mutation-Negative Erythrocytosis." Blood 116, no. 21 (2010): 4105. http://dx.doi.org/10.1182/blood.v116.21.4105.4105.

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Abstract Abstract 4105 Background: JAK2 mutations are found in approximately 99% of patients with polycythemia vera (PV) and 60% of those with essential thrombocythemia (ET) or primary myelofibrosis (PMF). It is currently assumed that other mutations relevant to JAK signaling contribute to the pathogenesis of JAK2 mutation-negative myeloproliferative neoplasms (MPN). The same might hold true for some cases of “idiopathic erythrocytosis” associated with subnormal serum erythropoietin level (sEpo). LNK is a plasma membrane-bound adaptor protein whose function includes inhibition of wild-type and

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17

Simon, Clotilde, Elisabetta Dondi, Amandine Chaix, et al. "Lnk adaptor protein down-regulates specific Kit-induced signaling pathways in primary mast cells." Blood 112, no. 10 (2008): 4039–47. http://dx.doi.org/10.1182/blood-2008-05-154849.

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Abstract Stem cell factor (SCF) plays critical roles in proliferation, survival, migration, and function of hematopoietic progenitor and mast cells through binding to Kit receptor. Previous studies have implicated the adaptor protein Lnk as an important negative regulator of SCF signaling. However, the molecular mechanism underlying this regulation is unclear. Here, we showed that the Src homology 2 domain (SH2) of Lnk binds directly and preferentially to phosphorylated tyrosine 567 in Kit juxtamembrane domain. Using Lnk−/− bone marrow mast cells (BMMCs) transduced with different Lnk proteins,

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18

Gueller, Saskia, Helen S. Goodridge, Hongtao Xing, Sigal Gery, Hubert Serve, and H. Phillip Koeffler. "Adaptor Protein Lnk Inhibits C-Fms Mediated Macrophage Function." Blood 112, no. 11 (2008): 3555. http://dx.doi.org/10.1182/blood.v112.11.3555.3555.

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Abstract The macrophage colony-stimulating factor receptor (c-Fms) plays an important role in proliferation, differentiation and survival of macrophages and is involved in the regulation of distinct macrophage functions. Interaction with the ligand M-CSF results in activation of the intracellular tyrosine kinase domain and phosphorylation of tyrosine residues, thereby creating binding sites for several molecules containing Src homology 2 (SH2) domains. One such protein is the adaptor Lnk that negatively regulates several hematopoietic cytokine receptors including MPL, EpoR and c-Kit. Lnk belon

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19

Gueller, Saskia, Sigal Gery, Verena Nowak, Liqin Liu, Hubert Serve, and H. Phillip Koeffler. "Adaptor protein Lnk associates with Tyr568 in c-Kit." Biochemical Journal 415, no. 2 (2008): 241–45. http://dx.doi.org/10.1042/bj20080102.

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The adaptor protein Lnk is expressed in haemopoietic cells and plays a critical role in haemopoiesis. Animal model studies demonstrated that Lnk acts as a broad inhibitor of signalling pathways in haemopoietic lineages. Lnk belongs to a family of proteins sharing several structural motifs, including an SH2 (Src homology 2) domain which binds phosphotyrosine residues in various signal-transducing proteins. The SH2 domain is essential for Lnk-mediated negative regulation of several cytokine receptors [e.g. Mpl, EpoR (erythropoietin receptor), c-Kit]. Therefore inhibition of the binding of Lnk to

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20

Eto, Koji, Hitoshi Takizawa, Hidekazu Nishikii, et al. "Negative Hematopoietic Scaffold Lnk Upregulates Integrin Outside-In Signaling in Platelets." Blood 106, no. 11 (2005): 382. http://dx.doi.org/10.1182/blood.v106.11.382.382.

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Abstract The adaptor molecule Lnk negatively regulates signaling downstream of cytokine receptors in self-renewal of hematopoietic stem cells, proliferation of B precursors and differentiation/maturation of megakaryocytes. The circulating number of platelets in Lnk-deficient mice is increased by 5-folds to control, presumably owing to its negative effects on TPO-elicited signaling. Lnk expression is maintained in platelets, however, the precise functions in platelets remain unknown. Here we report that Lnk deficiency results in the prolonged bleeding time (2-folds, p&lt;0.01) due to, at le

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21

Gery, Sigal, Saskia Gueller, Katya Chumakova, Norihiko Kawamata, Liqin Liu, and H. Phillip Koeffler. "Adaptor protein Lnk negatively regulates the mutant MPL, MPLW515L associated with myeloproliferative disorders." Blood 110, no. 9 (2007): 3360–64. http://dx.doi.org/10.1182/blood-2007-05-089326.

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Abstract Recently, activating myeloproliferative leukemia virus oncogene (MPL) mutations, MPLW515L/K, were described in myeloproliferative disorder (MPD) patients. MPLW515L leads to activation of downstream signaling pathways and cytokine-independent proliferation in hematopoietic cells. The adaptor protein Lnk is a negative regulator of several cytokine receptors, including MPL. We show that overexpression of Lnk in Ba/F3-MPLW515L cells inhibits cytokine-independent growth, while suppression of Lnk in UT7-MPLW515L cells enhances proliferation. Lnk blocks the activation of Jak2, Stat3, Erk, an

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22

Takizawa, Hitoshi, Chiyomi Kubo-Akashi, Ikuo Nobuhisa, et al. "Enhanced engraftment of hematopoietic stem/progenitor cells by the transient inhibition of an adaptor protein, Lnk." Blood 107, no. 7 (2006): 2968–75. http://dx.doi.org/10.1182/blood-2005-05-2138.

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AbstractHematopoietic stem cells (HSCs) are the key elements responsible for maintaining blood-cell production throughout life and for lymphohematopoietic reconstitution following bone marrow (BM) transplantation. Enhancement of the engrafting potential and expansion capabilities of HSCs as well as hematopoietic progenitor cells (HPCs) has been a long-time desire as a means of reducing the risks and difficulties that accompany BM transplantation. The ability of HSCs/HPCs to reconstitute the hematopoietic system of irradiated hosts is negatively regulated by an intracellular adaptor protein, Ln

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23

Tong, Wei, and Harvey F. Lodish. "Lnk Inhibits Tpo–mpl Signaling and Tpo-mediated Megakaryocytopoiesis." Journal of Experimental Medicine 200, no. 5 (2004): 569–80. http://dx.doi.org/10.1084/jem.20040762.

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Thrombopoietin (Tpo) is the primary cytokine regulating megakaryocyte development and platelet production. Tpo signaling through its receptor, c-mpl, activates multiple pathways including signal transducer and activator of transcription (STAT)3, STAT5, phosphoinositide 3-kinase–Akt, and p42/44 mitogen-activated protein kinase (MAPK). The adaptor protein Lnk is implicated in cytokine receptor and immunoreceptor signaling. Here, we show that Lnk overexpression negatively regulates Tpo-mediated cell proliferation and endomitosis in hematopoietic cell lines and primary hematopoietic cells. Lnk att

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24

Yano, Mio, Toshihiko Imamura, Kenichi Sakamoto, et al. "Clinical Significance of LNK (SH2B3) Expression in Pediatric B Cell Precursor Acute Lymphoblastic Leukemia." Blood 124, no. 21 (2014): 3772. http://dx.doi.org/10.1182/blood.v124.21.3772.3772.

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Abstract Background: In pediatric B cell precursor acute lymphoblastic leukemia (BCP-ALL), aberrant JAK-STAT signaling is one of the key leukemogenic mechanisms. Although activating mutations of JAK2 are found in high-risk BCP-ALL patients in western countries, such mutations are rare in Japanese cohorts, led to speculation of other factors contributing abnormal activation of JAK-STAT pathway. The adaptor protein LNK (SH2B3) is one of the negative regulator of JAK-STAT signaling, and its loss of function mutations have been identified in myeloproliferative neoplasms and high-risk BCP-ALL. In a

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25

Pérez-García, Pablo, Yuan Ma, Marcelo J. Yanovsky, and Paloma Mas. "Time-dependent sequestration of RVE8 by LNK proteins shapes the diurnal oscillation of anthocyanin biosynthesis." Proceedings of the National Academy of Sciences 112, no. 16 (2015): 5249–53. http://dx.doi.org/10.1073/pnas.1420792112.

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Circadian clocks sustain 24-h rhythms in physiology and metabolism that are synchronized with the day/night cycle. In plants, the regulatory network responsible for the generation of rhythms has been broadly investigated over the past years. However, little is known about the intersecting pathways that link the environmental signals with rhythms in cellular metabolism. Here, we examine the role of the circadian components REVEILLE8/LHY-CCA1-LIKE5 (RVE8/LCL5) and NIGHT LIGHT–INDUCIBLE AND CLOCK-REGULATED genes (LNK) shaping the diurnal oscillation of the anthocyanin metabolic pathway. Around da

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26

Komartin, Raluca Sanda, Brindusa Balanuca, Madalina Ioana Necolau, Anca Cojocaru, and Raluca Stan. "Composite Materials from Renewable Resources as Sustainable Corrosion Protection Coatings." Polymers 13, no. 21 (2021): 3792. http://dx.doi.org/10.3390/polym13213792.

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Epoxidized linseed oil (ELO) and kraft lignin (LnK) were used to obtain new sustainable composites as corrosion protection layers through a double-curing procedure involving UV radiation and thermal curing to ensure homogeneous distribution of the filler. The crosslinked structures were confirmed by Fourier-transform infrared spectrometry (FTIR), by comparative monitorization of the absorption band at 825 cm−1, attributed to the stretching vibration of epoxy rings. Thermal degradation behavior under N2 gas indicates that the higher LnK content, the better thermal stability of the composites (o

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27

Baran-Marszak, Fanny, Hajer Magdoud, Christophe Desterke, et al. "Expression level and differential JAK2-V617F–binding of the adaptor protein Lnk regulates JAK2-mediated signals in myeloproliferative neoplasms." Blood 116, no. 26 (2010): 5961–71. http://dx.doi.org/10.1182/blood-2009-12-256768.

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Abstract Activating mutations in signaling molecules, such as JAK2-V617F, have been associated with myeloproliferative neoplasms (MPNs). Mice lacking the inhibitory adaptor protein Lnk display deregulation of thrombopoietin/thrombopoietin receptor signaling pathways and exhibit similar myeloproliferative characteristics to those found in MPN patients, suggesting a role for Lnk in the molecular pathogenesis of these diseases. Here, we showed that LNK levels are up-regulated and correlate with an increase in the JAK2-V617F mutant allele burden in MPN patients. Using megakaryocytic cells, we demo

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Morris, Rhiannon, Liesl Butler, Andrew Perkins, Nadia J. Kershaw, and Jeffrey J. Babon. "The Role of LNK (SH2B3) in the Regulation of JAK-STAT Signalling in Haematopoiesis." Pharmaceuticals 15, no. 1 (2021): 24. http://dx.doi.org/10.3390/ph15010024.

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LNK is a member of the SH2B family of adaptor proteins and is a non-redundant regulator of cytokine signalling. Cytokines are secreted intercellular messengers that bind to specific receptors on the surface of target cells to activate the Janus Kinase-Signal Transducer and Activator of Transcription (JAK-STAT) signalling pathway. Activation of the JAK-STAT pathway leads to proliferative and often inflammatory effects, and so the amplitude and duration of signalling are tightly controlled. LNK binds phosphotyrosine residues to signalling proteins downstream of cytokines and constrains JAK-STAT

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Koren-Michowitz, Maya, Sigal Gery, Daniel Nowak, and Phillip H. Koeffler. "Adaptor Protein Lnk Binds to JAK3 and Negatively Regulates a Mutant Activating Allele Associated with Megakaryocytic Leukemia." Blood 114, no. 22 (2009): 5044. http://dx.doi.org/10.1182/blood.v114.22.5044.5044.

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Abstract Abstract 5044 The adaptor protein Lnk is known to associate with hematopoietic cytokine receptors such as cKIT, MPL and PDGFR, as well as, non-receptor tyrosine kinases such as JAK2, and is considered to have an inhibitory effect on these signaling pathways. JAK3 is expressed mainly in the hematopoietic system and its absence is associated with autosomal recessive severe combined immunodeficiency (SCID). Recently, activating mutations of JAK3 were described in transient myeloproliferative disorder (TMD) and acute megakaryocytic leukemia (AMKL) in Down syndrome (DS) patients as well as

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30

Lin, Dechen, Tong Yin, Maya koren-Michowitz, et al. "Adaptor Protein Lnk Binds to and Inhibits Normal and Leukemic FLT3." Blood 120, no. 21 (2012): 1312. http://dx.doi.org/10.1182/blood.v120.21.1312.1312.

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Abstract Abstract 1312 Background The production and lineage commitment of hematopoietic cells is controlled by the actions of a complex network of signaling pathways. Mutations and translocations of tyrosine kinases within these pathways lead to constitutive signaling and enhanced proliferation. Classic examples are BCR-ABL in CML, Janus kinase 2 (JAK2) mutations in MPN, Fms-like tyrosine kinase 3 (FLT3) and c-KIT mutations in AML. FLT3 is a receptor tyrosine kinase with important roles in hematopoietic progenitor cell survival and proliferation. It is mutated in about 1/3 of AML patients, mo

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Bersenev, Alexey, Chao Wu, Joanna Balcerek, and Wei Tong. "Lnk Constrains Oncogenic JAK2-Induced Myeloproliferative Disease in Mice." Blood 114, no. 22 (2009): 1437. http://dx.doi.org/10.1182/blood.v114.22.1437.1437.

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Abstract Abstract 1437 Poster Board I-460 Hematopoietic stem cell (HSC) homeostasis and self-renewal are regulated by intrinsic cytokine signaling pathways. One important signaling axis for HSC is the cell surface receptor, Mpl, and its ligand, thrombopoietin (Tpo). Upon Tpo stimulation, Mpl activates Janus Kinase (JAK2), which in turn triggers a cascade of downstream signal transduction pathways that regulate key aspects of cell development. Mice that lack the inhibitory adaptor protein Lnk harbor a vastly expanded HSC pool with enhanced self-renewal. We previously demonstrated that Lnk contr

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Cheng, Ying, Kudakwashe Chikwava, Chao Wu, Anchit Bhagat, John K. Choi, and Wei Tong. "LNK (SH2B3) Synergizes with TP53 in Suppressing B-Precursor Acute Lymphoblastic Leukemia through IL-7 Receptor Signaling." Blood 124, no. 21 (2014): 1074. http://dx.doi.org/10.1182/blood.v124.21.1074.1074.

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Abstract B-precursor acute lymphoblastic leukemia (B-ALL) is the leading cause of cancer-related deaths in children and commonly has a poor outcome in adults. Gene profiling and exome sequencing of high-risk ALLs led to the recent identification of the Philadelphia chromosome (Ph)-like ALL subtype. These leukemias have gene expression profiles similar to BCR-ABL1-positive (Ph+) ALL, but lack a BCR-ABL1 rearrangement, and often result in poor outcomes. Many Ph-like ALL-associated mutations identified to date are known or predicted to activate oncogenic cytokine receptor signaling pathways, part

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Bersenev, Alexey, Chao Wu, Joanna Balcerek, and Wei Tong. "Lnk Controls Hematopoietic Stem Cell Self-Renewal through Direct Interactions with JAK2 and Contributes to Oncogenic JAK2-Induced Myeloproliferative Diseases in Mice." Blood 112, no. 11 (2008): 895. http://dx.doi.org/10.1182/blood.v112.11.895.895.

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Abstract Hematopoietic stem cell (HSC) homeostasis and self-renewal are regulated by intrinsic cytokine signaling pathways. One important signaling axis for HSC is the cell surface receptor, Mpl, and its ligand, thrombopoietin (Tpo). Upon Tpo stimulation, Mpl activates Janus Kinase (JAK2) that triggers a cascade of downstream signal transduction pathways that regulates many aspects of cell development. Under steady-state conditions, mice lacking the inhibitory adaptor protein Lnk harbor an expanded HSC pool with enhanced self-renewal. Surprisingly, we found that Lnk−/− HSCs have an increased q

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34

Holdreith, Nicholas, Grace Lee, Vemika Chandra, et al. "LNK (SH2B3) inhibition expands healthy and Fanconi anemia human hematopoietic stem and progenitor cells." Blood Advances 6, no. 3 (2022): 731–45. http://dx.doi.org/10.1182/bloodadvances.2021004205.

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Abstract Hematopoietic stem cell transplantation (HSCT) remains the only curative treatment for a variety of hematological diseases. Allogenic HSCT requires hematopoietic stem cells (HSCs) from matched donors and comes with cytotoxicity and mortality. Recent advances in genome modification of HSCs have demonstrated the possibility of using autologous HSCT-based gene therapy to alleviate hematologic symptoms in monogenic diseases, such as the inherited bone marrow failure (BMF) syndrome Fanconi anemia (FA). However, for FA and other BMF syndromes, insufficient HSC numbers with functional defect

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35

Matsumoto, Tomoyuki, Masaaki Ii, Hiromi Nishimura, et al. "Lnk-dependent axis of SCF–cKit signal for osteogenesis in bone fracture healing." Journal of Experimental Medicine 207, no. 10 (2010): 2207–23. http://dx.doi.org/10.1084/jem.20100321.

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The therapeutic potential of hematopoietic stem cells/endothelial progenitor cells (HSCs/EPCs) for fracture healing has been demonstrated with evidence for enhanced vasculogenesis/angiogenesis and osteogenesis at the site of fracture. The adaptor protein Lnk has recently been identified as an essential inhibitor of stem cell factor (SCF)–cKit signaling during stem cell self-renewal, and Lnk-deficient mice demonstrate enhanced hematopoietic reconstitution. In this study, we investigated whether the loss of Lnk signaling enhances the regenerative response during fracture healing. Radiological an

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36

Gueller, Saskia, Sigal Gery, and H. Phillip Koeffler. "Adaptor Protein Lnk Binds to PDGFRA, PDGFRB and FIP1L1-PDGFRA, but Not to the TEL-PDGFRB Fusion Protein." Blood 110, no. 11 (2007): 2213. http://dx.doi.org/10.1182/blood.v110.11.2213.2213.

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Abstract PDGFRA and PDGFRB (platelet derived growth factor receptors alpha and beta) are frequently expressed on malignant hematopoietic cells and regulate various cellular responses such as development, proliferation, differentiation, cell survival and cellular transformation. Stimulation by either autocrine loops or constitutional activation by chromosomal translocation (i.e. chronic myelomonocytic leukemia [CMML, TEL-PDGFRB] or chronic eosinophilic leukemia [CEL, FIP1L1-PDGFRA]) makes them important factors in development of hematopoietic disorders. Normally, interaction with the ligand PDG

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37

Takaki, Satoshi, Hatsue Morita, Yoshinari Tezuka, and Kiyoshi Takatsu. "Enhanced Hematopoiesis by Hematopoietic Progenitor Cells Lacking Intracellular Adaptor Protein, Lnk." Journal of Experimental Medicine 195, no. 2 (2002): 151–60. http://dx.doi.org/10.1084/jem.20011170.

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Hematopoietic stem cells (HSCs) give rise to variety of hematopoietic cells via pluripotential progenitors and lineage-committed progenitors and are responsible for blood production throughout adult life. Amplification of HSCs or progenitors represents a potentially powerful approach to the treatment of various blood disorders and to applying gene therapy by bone marrow transplantation. Lnk is an adaptor protein regulating the production of B cells. Here we show that Lnk is also expressed in hematopoietic progenitors in bone marrow, and that in the absence of Lnk, the number and the hematopoie

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38

Wang, Wei, Yang Tang, Ying Wang, et al. "SH2B3/LNK Loss of Function Promotes Atherosclerosis and Thrombosis." Blood 126, no. 23 (2015): 3443. http://dx.doi.org/10.1182/blood.v126.23.3443.3443.

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Abstract Human genome-wide association studies (GWAS) have revealed many novel genetic loci that are associated with coronary heart disease (CHD) but do not involve traditional risk factors. However, the relevant genes and mechanisms are largely unknown. One such locus resides in SH2B3/LNK, which is expressed in hematopoietic cells and suppresses thrombopoietin (TPO) signaling via its receptor (MPL). The common risk single nucleotide polymorphism (SNP) of SH2B3/LNK is associated with CHD, increased platelet and myeloid cell counts in peripheral blood and JAK2V617F positive myeloproliferative n

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39

Bunting, Kevin D. "Another Lnk to STAT activation." Blood 116, no. 6 (2010): 862–64. http://dx.doi.org/10.1182/blood-2010-05-283176.

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McMullin, Mary Frances, and Holger Cario. "LNK mutations and myeloproliferative disorders." American Journal of Hematology 91, no. 2 (2016): 248–51. http://dx.doi.org/10.1002/ajh.24259.

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41

Oh, Stephen T., Jacob M. Zahn, Carol D. Jones, et al. "Identification of Novel LNK Mutations In Patients with Chronic Myeloproliferative Neoplasms and Related Disorders." Blood 116, no. 21 (2010): 315. http://dx.doi.org/10.1182/blood.v116.21.315.315.

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Abstract Abstract 315 Introduction: Dysregulated JAK-STAT signaling in chronic myeloproliferative neoplasms (MPNs) has primarily been attributed to activating mutations in tyrosine kinases. However, JAK-STAT activation can be demonstrated in some patients lacking JAK2 or MPL mutations, suggesting alteration of other regulatory elements in this pathway. One regulator of JAK-STAT signaling is LNK (SH2B3), an adapter protein that contains a proline-rich N-terminal dimerization domain (Pro/DD), a pleckstrin homology (PH) domain (plasma membrane localization), and an SH2 domain. LNK binds to cytoki

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42

Norddahl, Gudmundur L., Martin Wahlestedt, Santiago Gisler, Mikael Sigvardsson, and David Bryder. "Enhanced Cytokine Responsiveness Counteracts Age-Induced Decline in Hematopoietic Stem Cell Function." Blood 118, no. 21 (2011): 2342. http://dx.doi.org/10.1182/blood.v118.21.2342.2342.

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Abstract Abstract 2342 In recent years, it has become increasingly clear that physiologic aging has several profound cell intrinsic effects on hematopoietic stem cell (HSC) aging. This includes an altered output of mature progeny and an expansion of the HSC pool, although the latter is accompanied with several functional shortcomings. Because of the hierarchical structure of hematopoiesis, improving HSC function should present a promising avenue to restore aberrant hematopoietic function. The signal adaptor protein Lnk, a relay of cytokine signaling, has been shown to negatively regulate hemat

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43

López-Mejía, José A., Jessica C. Mantilla-Ollarves, and Leticia Rocha-Zavaleta. "Modulation of JAK-STAT Signaling by LNK: A Forgotten Oncogenic Pathway in Hormone Receptor-Positive Breast Cancer." International Journal of Molecular Sciences 24, no. 19 (2023): 14777. http://dx.doi.org/10.3390/ijms241914777.

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Breast cancer remains the most frequently diagnosed cancer in women worldwide. Tumors that express hormone receptors account for 75% of all cases. Understanding alternative signaling cascades is important for finding new therapeutic targets for hormone receptor-positive breast cancer patients. JAK-STAT signaling is commonly activated in hormone receptor-positive breast tumors, inducing inflammation, proliferation, migration, and treatment resistance in cancer cells. In hormone receptor-positive breast cancer, the JAK-STAT cascade is stimulated by hormones and cytokines, such as prolactin and I

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44

Singh, Brijendra, Carlo Salas Salinas, Md Akram Hossain, Christopher Millington, Ketan Patel, and Wei Tong. "Reducing DNA Damage Associated with Endogenous Genotoxic Stress in Hematopoietic Stem Cells." Blood 142, Supplement 1 (2023): 1361. http://dx.doi.org/10.1182/blood-2023-188029.

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Fanconi anemia (FA) is a bone marrow failure (BMF) syndrome that arises from mutations in a network of FA genes essential for DNA interstrand crosslink (ICL) repair and replication stress tolerance. Endogenous formaldehyde is ubiquitous within cells as it is produced as a byproduct during normal cellular metabolism such as histone, RNA and DNA demethylation. Previous studies show that endogenous formaldehyde is a hematopoietic stem cell (HSC) genotoxin and metabolic carcinogen. We previously showed that endogenous formaldehyde is removed by the enzyme alcohol dehydrogenase 5 (ADH5), and Adh5-d

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45

Oh, Stephen T., Erin F. Simonds, Carol Jones, et al. "Novel mutations in the inhibitory adaptor protein LNK drive JAK-STAT signaling in patients with myeloproliferative neoplasms." Blood 116, no. 6 (2010): 988–92. http://dx.doi.org/10.1182/blood-2010-02-270108.

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Abstract Dysregulated Janus kinase–signal transducer and activator of transcription (JAK-STAT) signaling due to activation of tyrosine kinases is a common feature of myeloid malignancies. Here we report the first human disease-related mutations in the adaptor protein LNK, a negative regulator of JAK-STAT signaling, in 2 patients with JAK2 V617F–negative myeloproliferative neoplasms (MPNs). One patient exhibited a 5 base-pair deletion and missense mutation leading to a premature stop codon and loss of the pleckstrin homology (PH) and Src homology 2 (SH2) domains. A second patient had a missense

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46

Rumi, Elisa, Ashot S. Harutyunyan, Daniela Pietra, et al. "LNK mutations in familial myeloproliferative neoplasms." Blood 128, no. 1 (2016): 144–45. http://dx.doi.org/10.1182/blood-2016-04-711150.

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47

Bersenev, Alexey, Chao Wu, Joanna Balcerek, et al. "Lnk constrains myeloproliferative diseases in mice." Journal of Clinical Investigation 120, no. 6 (2010): 2058–69. http://dx.doi.org/10.1172/jci42032.

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48

Ema, Hideo, Jun Seita, Jun Ooehara, Akiko Iseki, Hina Takano, and Hiromitsu Nakauchi. "Adaptor Protein Lnk Negatively Controls the Likelihood of Self-Renewal in Hematopoietic Stem Cells." Blood 108, no. 11 (2006): 1316. http://dx.doi.org/10.1182/blood.v108.11.1316.1316.

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Abstract Great progresses are promised for the development of stem cell-based regenerative medicine if we can manipulate stem cell self-renewal. Thus, one of the central tasks in stem cell biology is to understand how stem cell fate is determined. Hematopoietic stem cells (HSCs) are the best studied stem cells. Their in vivo self-renewal has been extensively studied, but its in vitro recapitulation remains so difficult. We previously reported that HSCs undergo asymmetrical self-renewal division in culture with stem cell factor (SCF) and thrombopoietin (TPO). Since then, we have sought any cond

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49

Vila González, Patricia Elizabet, and María Noel Pereyra. "Interpretación a partir del análisis cinético de los resultados del ensayo acelerado (IRAM 1674) para la reacción álcali-sílice pavimentos." Métodos y Materiales 7 (May 22, 2018): 1–10. http://dx.doi.org/10.15517/mym.v7i1.29716.

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En este trabajo se presentan los resultados de expansión según el ensayo acelerado de la barra de mortero (IRAM 1674) hasta los 14 días de inmersión en solución agresiva y el análisis cinético según las recomendaciones RILEM AAR-2. El objetivo principal del trabajo es contribuir a la interpretación de los resultados del ensayo acelerado a partir del análisis del crecimiento de la expansión con la edad del ensayo (análisis cinético), otorgándole así mayor confiabilidad al ensayo. El análisis cinético consiste en ajustar por mínimos cuadrados los datos experimentales de expansión a un modelo de

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50

Balcerek, Joanna, Jing Jiang, Qinqin Jiang, Kaosheng Lyu, Roger Greenberg, and Wei Tong. "LNK (SH2B3) Deficiency Ameliorates Hematopoietic Stem Cell Defects in Fanconi Anemi." Blood 128, no. 22 (2016): 2670. http://dx.doi.org/10.1182/blood.v128.22.2670.2670.

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Abstract Fanconi Anemia (FA) is one of the most common inherited bone marrow failure (iBMF) syndromes. Although initially identified over 85 years ago, FA remains a fatal genetic disease. Nineteen FA genes cooperate in a genome stability pathway that is essential for repair of DNA damage and tolerance of replication stress. Cells derived from FA patients are hypersensitive to DNA interstrand crosslink (ICL)-inducing agents, such as Mitomycin C (MMC), and exhibit DNA damage checkpoint and mitosis defects. Mutations in FA genes result in hematopoietic stem cell (HSC) defects, bone marrow failure

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