Relevant bibliographies by topics / Ack1

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Ack1'

Author: Grafiati
Published: 4 June 2021
Last updated: 10 February 2022

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Journal articles on the topic "Ack1"

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Lin, Qiong, Jian Wang, Chandra Childress, and Wannian Yang. "The activation mechanism of ACK1 (activated Cdc42-associated tyrosine kinase 1)." Biochemical Journal 445, no. 2 (June 27, 2012): 255–64. http://dx.doi.org/10.1042/bj20111575.

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ACK [activated Cdc42 (cell division cycle 42)-associated tyrosine kinase; also called TNK2 (tyrosine kinase, non-receptor, 2)] is activated in response to multiple cellular signals, including cell adhesion, growth factor receptors and heterotrimeric G-protein-coupled receptor signalling. However, the molecular mechanism underlying activation of ACK remains largely unclear. In the present study, we demonstrated that interaction of the SH3 (Src homology 3) domain with the EBD [EGFR (epidermal growth factor receptor)-binding domain] in ACK1 forms an auto-inhibition of the kinase activity. Release of this auto-inhibition is a key step for activation of ACK1. Mutation of the SH3 domain caused activation of ACK1, independent of cell adhesion, suggesting that cell adhesion-mediated activation of ACK1 is through releasing the auto-inhibition. A region at the N-terminus of ACK1 (Leu10–Leu14) is essential for cell adhesion-mediated activation. In the activation of ACK1 by EGFR signalling, Grb2 (growth-factor-receptor-bound protein 2) mediates the interaction of ACK1 with EGFR through binding to the EBD and activates ACK1 by releasing the auto-inhibition. Furthermore, we found that mutation of Ser445 to proline caused constitutive activation of ACK1. Taken together, our studies have revealed a novel molecular mechanism underlying activation of ACK1.
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Shen, Feng, Qiong Lin, Yan Gu, Chandra Childress, and Wannian Yang. "Activated Cdc42-associated Kinase 1 Is a Component of EGF Receptor Signaling Complex and Regulates EGF Receptor Degradation." Molecular Biology of the Cell 18, no. 3 (March 2007): 732–42. http://dx.doi.org/10.1091/mbc.e06-02-0142.

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Cdc42-associated tyrosine kinase 1 (ACK1) is a specific down-stream effector of Cdc42, a Rho family small G-protein. Previous studies have shown that ACK1 interacts with clathrin heavy chain and is involved in clathrin-coated vesicle endocytosis. Here we report that ACK1 interacted with epidermal growth factor receptor (EGFR) upon EGF stimulation via a region at carboxy terminus that is highly homologous to Gene-33/Mig-6/RALT. The interaction of ACK1 with EGFR was dependent on the kinase activity or tyrosine phosphorylation of EGFR. Immunofluorescent staining using anti-EGFR and GFP-ACK1 indicates that ACK1 was colocalized with EGFR on EEA-1 positive vesicles upon EGF stimulation. Suppression of the expression of ACK1 by ACK-RNAi inhibited ligand-induced degradation of EGFR upon EGF stimulation, suggesting that ACK1 plays an important role in regulation of EGFR degradation in cells. Furthermore, we identified ACK1 as an ubiquitin-binding protein. Through an ubiquitin-association (Uba) domain at the carboxy terminus, ACK1 binds to both poly- and mono-ubiquitin. Overexpression of the Uba domain-deletion mutant of ACK1 blocked the ligand-dependent degradation of EGFR, suggesting that ACK1 regulates EGFR degradation via its Uba domain. Taken together, our studies suggest that ACK1 senses signal of EGF and regulates ligand-induced degradation of EGFR.
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Prieto-Echagüe, Victoria, and W. Todd Miller. "Regulation of Ack-Family Nonreceptor Tyrosine Kinases." Journal of Signal Transduction 2011 (February 17, 2011): 1–9. http://dx.doi.org/10.1155/2011/742372.

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Ack family non-receptor tyrosine kinases are unique with regard to their domain composition and regulatory properties. Human Ack1 (activated Cdc42-associated kinase) is ubiquitously expressed and is activated by signals that include growth factors and integrin-mediated cell adhesion. Stimulation leads to Ack1 autophosphorylation and to phosphorylation of additional residues in the C-terminus. The N-terminal SAM domain is required for full activation. Ack1 exerts some of its effects via protein-protein interactions that are independent of its kinase activity. In the basal state, Ack1 activity is suppressed by an intramolecular interaction between the catalytic domain and the C-terminal region. Inappropriate Ack1 activation and signaling has been implicated in the development, progression, and metastasis of several forms of cancer. Thus, there is increasing interest in Ack1 as a drug target, and studies of the regulatory properties of the enzyme may reveal features that can be exploited in inhibitor design.
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Chan, Wing, Soon-Tuck Sit, and Ed Manser. "The Cdc42-associated kinase ACK1 is not autoinhibited but requires Src for activation." Biochemical Journal 435, no. 2 (March 29, 2011): 355–64. http://dx.doi.org/10.1042/bj20102156.

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The non-RTK (receptor tyrosine kinase) ACK1 [activated Cdc42 (cell division cycle 42)-associated kinase 1] binds a number of RTKs and is associated with their endocytosis and turnover. Its mode of activation is not well established, but models have suggested that this is an autoinhibited kinase. Point mutations in its SH3 (Src homology 3)- or EGF (epidermal growth factor)-binding domains have been reported to activate ACK1, but we find neither of the corresponding W424K or F820A mutations do so. Indeed, deletion of the various ACK1 domains C-terminal to the catalytic domain are not associated with increased activity. A previous report identified only one major tyrosine phosphorylated protein of 60 kDa co-purified with ACK1. In a screen for new SH3 partners for ACK1 we found multiple Src family kinases; of these c-Src itself binds best. The SH2 and SH3 domains of Src interact with ACK1 Tyr518 and residues 623–652 respectively. Src targets the ACK1 activation loop Tyr284, a poor autophosphorylation site. We propose that ACK1 fails to undergo significant autophosphorylation on Tyr284in vivo because it is basophilic (whereas Src is acidophilic). Subsequent ACK1 activation downstream of receptors such as EGFR (EGF receptor) (and Src) promotes turnover of ACK1 in vivo, which is blocked by Src inhibitors, and is compromised in the Src-deficient SYF cell line. The results of the present study can explain why ACK1 is responsive to so many external stimuli including RTKs and integrin ligation, since Src kinases are commonly recruited by multiple receptor systems.
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Liu, Xia, Xuan Wang, Lifang Li, and Baolin Han. "Research Progress of the Functional Role of ACK1 in Breast Cancer." BioMed Research International 2019 (October 20, 2019): 1–6. http://dx.doi.org/10.1155/2019/1018034.

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ACK1 is a nonreceptor tyrosine kinase with a unique structure, which is tightly related to the biological behavior of tumors. Previous studies have demonstrated that ACK1 was involved with multiple signaling pathways of tumor progression. Its crucial role in tumor cell proliferation, apoptosis, invasion, and metastasis was tightly related to the prognosis and clinicopathology of cancer. ACK1 has a unique way of regulating cellular pathways, different from other nonreceptor tyrosine kinases. As an oncogenic kinase, recent studies have shown that ACK1 plays a critical regulatory role in the initiation and progression of tumors. In this review, we will be summarizing the structural characteristics, activation, and regulation of ACK1 in breast cancer, aiming to deeply understand the functional and mechanistic role of ACK1 and provide novel therapeutic strategies for breast cancer treatment.
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Wu, Sijia, Karl D. Bellve, Kevin E. Fogarty, and Haley E. Melikian. "Ack1 is a dopamine transporter endocytic brake that rescues a trafficking-dysregulated ADHD coding variant." Proceedings of the National Academy of Sciences 112, no. 50 (November 30, 2015): 15480–85. http://dx.doi.org/10.1073/pnas.1512957112.

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The dopamine (DA) transporter (DAT) facilitates high-affinity presynaptic DA reuptake that temporally and spatially constrains DA neurotransmission. Aberrant DAT function is implicated in attention-deficit/hyperactivity disorder and autism spectrum disorder. DAT is a major psychostimulant target, and psychostimulant reward strictly requires binding to DAT. DAT function is acutely modulated by dynamic membrane trafficking at the presynaptic terminal and a PKC-sensitive negative endocytic mechanism, or “endocytic brake,” controls DAT plasma membrane stability. However, the molecular basis for the DAT endocytic brake is unknown, and it is unknown whether this braking mechanism is unique to DAT or common to monoamine transporters. Here, we report that the cdc42-activated, nonreceptor tyrosine kinase, Ack1, is a DAT endocytic brake that stabilizes DAT at the plasma membrane and is released in response to PKC activation. Pharmacologic and shRNA-mediated Ack1 silencing enhanced basal DAT internalization and blocked PKC-stimulated DAT internalization, but had no effects on SERT endocytosis. Both cdc42 activation and PKC stimulation converge on Ack1 to control Ack1 activity and DAT endocytic capacity, and Ack1 inactivation is required for stimulated DAT internalization downstream of PKC activation. Moreover, constitutive Ack1 activation is sufficient to rescue the gain-of-function endocytic phenotype exhibited by the ADHD DAT coding variant, R615C. These findings reveal a unique endocytic control switch that is highly specific for DAT. Moreover, the ability to rescue the DAT(R615C) coding variant suggests that manipulating DAT trafficking mechanisms may be a potential therapeutic approach to correct DAT coding variants that exhibit trafficking dysregulation.
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Gajiwala, Ketan S., Karen Maegley, RoseAnn Ferre, You-Ai He, and Xiu Yu. "Ack1: Activation and Regulation by Allostery." PLoS ONE 8, no. 1 (January 14, 2013): e53994. http://dx.doi.org/10.1371/journal.pone.0053994.

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Furlow, Bryant. "Tyrosine kinase ACK1 promotes prostate tumorigenesis." Lancet Oncology 7, no. 1 (January 2006): 17. http://dx.doi.org/10.1016/s1470-2045(05)70525-8.

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del Mar Masdeu, Maria, Beatriz G. Armendáriz, Anna La Torre, Eduardo Soriano, Ferran Burgaya, and Jesús Mariano Ureña. "Identification of novel Ack1-interacting proteins and Ack1 phosphorylated sites in mouse brain by mass spectrometry." Oncotarget 8, no. 60 (September 15, 2017): 101146–57. http://dx.doi.org/10.18632/oncotarget.20929.

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Mahajan, Nupam P., Young E. Whang, James L. Mohler, and H. Shelton Earp. "Activated Tyrosine Kinase Ack1 Promotes Prostate Tumorigenesis: Role of Ack1 in Polyubiquitination of Tumor Suppressor Wwox." Cancer Research 65, no. 22 (November 15, 2005): 10514–23. http://dx.doi.org/10.1158/0008-5472.can-05-1127.

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Dissertations / Theses on the topic "Ack1"

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Vicente-García, José Julio. "Identification of new activated Cdc42 kinase (ACK1) binding proteins and characterisation of the ACK1-STAT3 interaction." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611738.

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Linderoth, E. "The role of Ack1 in TRAIL receptor signalling." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1369879/.

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The Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) is one of the most recently identified death inducing ligands of the TNF cytokine family. TRAIL induces apoptosis in most cancer cells, whereas the majority of normal cells are resistant. TRAIL receptor agonists are therefore considered to be a promising anti-cancer therapeutic. However, because many cancer cells develop resistance to TRAIL, understanding the mechanisms by which resistance is acquired will be critical for the therapeutic use of TRAIL in cancer therapy. We have discovered that Activated Cdc42-associated kinase 1 (Ack1) is required for TRAIL induced apoptosis in human epithelial cells. Ack1 is a non- receptor tyrosine kinase with numerous protein-protein interaction domains, suggested to have a role in several cellular processes such as trafficking, endocytosis and cell motility. Knockdown of Ack1 in various epithelial cell lines leads to significantly impaired TRAIL induced apoptosis as evident by reduced cleavage of Caspase-8 and -3 and surface exposure of phosphatidylserine. Exploring the underlying mechanism we found that Ack1 knockdown leads to impaired TRAIL induced clustering of TRAIL-R1 and a reduction in the recruitment of Caspase-8 to the DISC complex, essential for death inducing signal transduction. Translocation of the TRAIL receptors to lipid rafts in the plasma membrane have been suggested to be crucial for TRAIL receptor dynamics and downstream signalling following TRAIL ligand binding. In this work we show that Ack1 is required for the translocation of the TRAIL receptors to the lipid rafts. In this thesis, a novel regulatory role of Ack1 in apoptosis, death receptor signalling and lipid raft trafficking is presented, contributing further to the understanding of the molecular regulation of TRAIL receptor signalling.
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Svensson, Julia. "The Effects of ACK1 and Cell Density on ErbB3." Thesis, Uppsala universitet, Institutionen för biologisk grundutbildning, 2021. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-446027.

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The ErbB family of receptors are involved in signalling relating to cell proliferation and differentiation through activation of pathways such as PI3K and MAPK. Their overexpression is often found in different cancer types and therefore, their expression is under tight regulation. The ErbB family includes, EGFR, ErbB2, ErbB3, and ErbB4 where all but ErbB3 has a kinase domain, making ErbB3 a pseudokinase. Upon activation of the receptors, they are endocytosed through the formation of a clathrin-coated pit and are degraded in the lysosome. Interestingly, researchers have found that newly synthesised ErbB3 can also be degraded in the proteasome by protein Nrdp1. Suggesting that ErbB3 might work in a ligand-independent manner and needs additional regulatory mechanisms. ACK1 is a non-receptor tyrosine kinase that has a reported effect on EGFR by promoting receptor degradation in the autophagosome. However, their role in EGFR regulation is still debated. Therefore, this information alludes to the fact that ACK1 might influence other ErbB family members as well.   This report aims to investigate whether ACK1 influences ErbB3 levels. Through RNAi mediated knockdown of ACK1 in MCF10A cells, a novel role of ACK1 acting as a regulator of ErbB3 is hinted at. Surprisingly, these results also show that ACK1 seems to act specifically on ErbB3 and not on its family members, EGFR and ErbB2. Moreover, this report shows that ErbB3 expression is linked to cell density.
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Krawczyk, Sylwia. "The roles of Ack1 in growth factor signalling and trafficking." Thesis, University of Birmingham, 2014. http://etheses.bham.ac.uk//id/eprint/4775/.

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Growth factor signalling controls multiple cellular functions, such as cell growth, proliferation, migration and cell survival, and misregulation of growth factor signalling has been shown to promote cancer development and progression. The study presented within this thesis focuses on the functions of a non-receptor tyrosine kinase Ack1 (Activated Cdc42-associated kinase 1, TNK2) in epidermal growth factor (EGF) receptor (EGFR) trafficking. This study reveals that Ack1 subcellular localization greatly depends on EGF availability. Furthermore, this work also identifies a potential role for Ack1 in a non-canonical degradative pathway through its associations with several autophagosomal proteins. Analyses of a panel of the Ack1 deletion mutants further reveal key mechanistic aspects of these associations and identify the Ack1 domains which are required for these to occur. Finally, a mass spectrometric approach has been applied which identifies novel post-translational modification sites within Ack1, and in combination with stable isotope labelling of amino acids in cell culture (SILAC), has allowed for characterisation of novel Ack1 interactors.
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Wu, Sijia. "Novel Mechanisms Regulating Dopamine Transporter Endocytic Trafficking: Ack1-Controlled Endocytosis And Retromer-Mediated Recycling." eScholarship@UMMS, 2001. http://escholarship.umassmed.edu/gsbs_diss/887.

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Dopamine transporters (DAT) facilitate high-affinity presynaptic dopamine (DA) reuptake in the central nervous system, and are required to constrain extracellular DA levels and maintain presynaptic DAergic tone. DAT is the primary target for addictive and therapeutic psychostimulants, which require DAT binding to elicit reward. DAT availability at presynaptic terminals ensures its proper function, and is dynamically regulated by endocytic trafficking. My thesis research focused on two fundamental questions: 1) what are the molecular mechanisms that control DAT endocytosis? and 2) what are the mechanism(s) that govern DAT’s post-endocytic fate? Using pharmacological and genetic approaches, I discovered that a non-receptor tyrosine kinase, activated by cdc42 kinase 1 (Ack1), stabilizes DAT plasma membrane expression by negatively regulating DAT endocytosis. I found that stimulated DAT endocytosis absolutely requires Ack1 inactivation. Moreover, I was able to restore normal DAT endocytosis to a trafficking dysregulated DAT coding variant identified in an Attention Deficit Hyperactivity Disorder (ADHD) patient via constitutively activating Ack1. To address what mechanisms govern DAT’s post-endocytic fate, I took advantage of a small molecule labeling approach to directly couple fluorophore to the DAT surface population, and subsequently tracked DAT’s temporal-spatial post-endocytic itinerary in immortalized mesencephalic cells. Using this approach, I discovered that the retromer complex mediates DAT recycling and is required to maintain DAT surface levels via a DAT C-terminal PDZ-binding motif. Taken together, these findings shed considerable new light on DAT trafficking mechanisms, and pave the way for future studies examining the role of regulated DAT trafficking in neuropsychiatric disorders.
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Wu, Sijia. "Novel Mechanisms Regulating Dopamine Transporter Endocytic Trafficking: Ack1-Controlled Endocytosis And Retromer-Mediated Recycling." eScholarship@UMMS, 2017. https://escholarship.umassmed.edu/gsbs_diss/887.

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Dopamine transporters (DAT) facilitate high-affinity presynaptic dopamine (DA) reuptake in the central nervous system, and are required to constrain extracellular DA levels and maintain presynaptic DAergic tone. DAT is the primary target for addictive and therapeutic psychostimulants, which require DAT binding to elicit reward. DAT availability at presynaptic terminals ensures its proper function, and is dynamically regulated by endocytic trafficking. My thesis research focused on two fundamental questions: 1) what are the molecular mechanisms that control DAT endocytosis? and 2) what are the mechanism(s) that govern DAT’s post-endocytic fate? Using pharmacological and genetic approaches, I discovered that a non-receptor tyrosine kinase, activated by cdc42 kinase 1 (Ack1), stabilizes DAT plasma membrane expression by negatively regulating DAT endocytosis. I found that stimulated DAT endocytosis absolutely requires Ack1 inactivation. Moreover, I was able to restore normal DAT endocytosis to a trafficking dysregulated DAT coding variant identified in an Attention Deficit Hyperactivity Disorder (ADHD) patient via constitutively activating Ack1. To address what mechanisms govern DAT’s post-endocytic fate, I took advantage of a small molecule labeling approach to directly couple fluorophore to the DAT surface population, and subsequently tracked DAT’s temporal-spatial post-endocytic itinerary in immortalized mesencephalic cells. Using this approach, I discovered that the retromer complex mediates DAT recycling and is required to maintain DAT surface levels via a DAT C-terminal PDZ-binding motif. Taken together, these findings shed considerable new light on DAT trafficking mechanisms, and pave the way for future studies examining the role of regulated DAT trafficking in neuropsychiatric disorders.
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Krishnan, Kadalmani. "Characterisation of the G protein controlled tyrosine kinase, ACK1 and its interaction with nucleolar partner proteins." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610698.

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Cebula, Patricia Verfasser], Johannes [Akademischer Betreuer] Bode, and Dieter [Akademischer Betreuer] [Willbold. "HCV interferiert mit Ack1-abhängigen Signalwegen durch Herabregulation der TC-PTP / Patricia Cebula. Gutachter: Johannes Bode ; Dieter Willbold." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2011. http://d-nb.info/1015434118/34.

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Cebula, Patricia [Verfasser], Johannes Akademischer Betreuer] Bode, and Dieter [Akademischer Betreuer] [Willbold. "HCV interferiert mit Ack1-abhängigen Signalwegen durch Herabregulation der TC-PTP / Patricia Cebula. Gutachter: Johannes Bode ; Dieter Willbold." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2011. http://d-nb.info/1015434118/34.

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Guillet, Stéphanie. "Monogenic predisposition to systemic lupus erythematosus and efferocytosis Impaired efferocytosis and Systemic Lupus Erythematosus in patients with autosomal recessive ACK1 and BRK Kinases deficiencies." Thesis, Sorbonne Paris Cité, 2019. http://www.theses.fr/2019USPCB003.

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Le Lupus Erythemateux disséminé (LED) est un ensemble de maladies auto-immunes caractérisées par la présence d'anticorps anti-nucléaires. La pathogenèse du lupus est inconnue à ce jour et les mécanismes de la maladie pourraient être multiples. Dans ce travail nous reportons l'identification de variants autosomaux récessifs, pertes de function, dans le domaine kinase de ACK1 et BRK respectivement, chez des patients atteints de LED de 2 familles non apparentées. Utilisant des macrophages dérivés d'iPSCs similaires aux macrophages résidents exprimant TIM4, nous montrons que la forme sauvage de ACK1 et BRK n'est pas requise pour la phagocytose de bactéries et de champignons, mais est nécessaire pour une efferocytose efficace, incluant la phagocytose mediée par l'actin de cellules apoptotiques par des macrophages humains et l'expression précoce de gène anti-inflammatoire induit par STAT3 et AKT et déclenché par l'exposition à des cellules apoptotiques. Ces résultats indiquent que l'activité kinase de ACK1 et BRK sont nécessaires pour la clearance immunologiquement silencieuse des cellules apoptotiques par les macrophages. Enfin ces données définissent un sous-groupe de patients atteints de LED avec un déficit génétique d'efferocytose qui pourrait bénéficier de thérapie ciblée dans le future
Systemic Lupus Erythematosus (SLE) is a collection of autoimmune diseases characterized by auto-antibodies against nuclear antigens. Pathogenesis of SLE remains unclear and disease mechanisms may be multiple. Here we report the identification of autosomal recessive loss-of-function variants in the kinase domain of ACK1 and BRK, in patients from two families with SLE. Using patients and controls iPSC-derived Tim4+ resident-like macrophages we find that wild-type ACK1 and BRK are dispensable for phagocytosis of bacteria and fungi, but are both required for efficient efferocytosis, including actin-mediated engulfment of apoptotic cells by human macrophages, and an early cell-autonomous anti-inflammatory gene expression program driven by AKT and STAT3 and triggered by apoptotic cells. These results indicate that ACK1 and BRK kinases activity are required for the immunologically silent clearance of apoptotic cells by macrophages and define genetic efferocytosis deficiency in a subset of SLE patients who may benefit from personalized therapy in the future
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Books on the topic "Ack1"

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-Ack as in snack. Edina, Minn: SandCastle, 2003.

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Pelta, Eleanor. AILA's focus on immigration practice under AC21. Washington, D.C: American Immigrant Lawyers Association, 2009.

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1946-, Brown Richard E., ed. A snack for Mack: -ack. New York, N.Y: Scholastic, 2002.

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Bruce, J. M. AW FK. 3 (Little Ack). Berkhamsted: Albatros Publications, 1998.

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Brian, Butler, ed. Peter Robinson: Ack and other abdications. Auckland, N.Z: Clouds, 2010.

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Hoena, B. A. Eek and Ack vs the Wolfman. Minneapolis: Stone Arch Books, 2009.

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Hoena, B. A. Eek & Ack, the puzzling Pluto plot. Minneapolis, Minn: Stone Arch Books, 2008.

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ill, Winter Susan, ed. Acka backa boo!: Playground games from around the world. New York: H. Holt, 2000.

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Ack Värmeland: Regionalitet i diskurs och praktik. Göteborg: Etnologiska institutionen, Göteborgs universitet, 2000., 2000.

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The big mistake. London: Raintree, 2014.

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Book chapters on the topic "Ack1"

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Biswas-Fiss, Esther E., Stephanie Affet, Malissa Ha, Takaya Satoh, Joe B. Blumer, Stephen M. Lanier, Ana Kasirer-Friede, et al. "ACK1." In Encyclopedia of Signaling Molecules, 28–33. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_475.

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Takenaka, Nobuyuki, and Takaya Satoh. "ACK1." In Encyclopedia of Signaling Molecules, 102–8. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_475.

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Takenaka, Nobuyuki, and Takaya Satoh. "ACK1." In Encyclopedia of Signaling Molecules, 1–8. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_475-1.

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Beckner, Mark. "Adapters, AS2, and Acks." In BizTalk 2013 EDI for Health Care, 61–82. Berkeley, CA: Apress, 2014. http://dx.doi.org/10.1007/978-1-4302-6608-2_5.

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Beckner, Mark. "Adapters, AS2, and Acks." In BizTalk 2013 EDI for Supply Chain Management, 57–78. Berkeley, CA: Apress, 2013. http://dx.doi.org/10.1007/978-1-4302-6344-9_5.

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Biggs, Catherine M., and Stuart E. Turvey. "Chronic Mucocutaneous Candidiasis, ACT1 Deficiency." In Encyclopedia of Medical Immunology, 1–4. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4614-9209-2_63-1.

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Biggs, Catherine M., and Stuart E. Turvey. "Chronic Mucocutaneous Candidiasis, ACT1 Deficiency." In Encyclopedia of Medical Immunology, 161–64. New York, NY: Springer New York, 2020. http://dx.doi.org/10.1007/978-1-4614-8678-7_63.

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Abramov, Raz, and Amir Herzberg. "TCP Ack Storm DoS Attacks." In IFIP Advances in Information and Communication Technology, 29–40. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-21424-0_3.

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Jouannaud, Jean-Pierre, and Claude Marché. "Completion modulo associativity, commutativity and identity (AC1)." In Design and Implementation of Symbolic Computation Systems, 111–20. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/3-540-52531-9_130.

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Domenjoud, Eric. "AC unification through order-sorted AC1 unification." In Rewriting Techniques and Applications, 98–111. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/3-540-53904-2_89.

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Conference papers on the topic "Ack1"

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Albertella, Mark, Shilina Roman, Mike Briggs, Aaron Cranston, Ralph Graeser, George Hynd, David Jones, et al. "Abstract A143: A preclinical in vivo model to assess pharmacodynamic inhibition of ACK1." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-a143.

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PHATAK, SHARANGDHAR S., and SHUXING ZHANG. "A NOVEL MULTI-MODAL DRUG REPURPOSING APPROACH FOR IDENTIFICATION OF POTENT ACK1 INHIBITORS." In Proceedings of the Pacific Symposium. WORLD SCIENTIFIC, 2012. http://dx.doi.org/10.1142/9789814447973_0004.

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Mahajan, Kiran, Sayantani Bandyopadhyay, and Nupam Mahajan. "Abstract 2599: KDM3A tyrosine phosphorylation by Ack1 promotes tamoxifen-resistance in breast cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2599.

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Balasooriyage, Eranga Roshan Balasooriya Loku, Jacob Owen, Jack Gashler, Colin Muir, Katie Pennington, James Moody, and Joshua L. Andersen. "Abstract 2304: Regulation of the oncogenic tyrosine kinase ACK1 through ubiquitin-dependent mechanism." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2304.

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Zhang, Zhentao, Dinuka De Silva, Yuanbo Liu, H. Shelton Earp, and Young E. Whang. "Abstract 4533: Interaction between androgen receptor and its corepressor SLIRP is regulated by Ack1 tyrosine kinase." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4533.

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Lawrence, Harshani R., Yunting Luo, Daniel Zhang, Nathan Tindall, Sevil Ozcan, Miles Huseyin, Sakib Kazi, et al. "Abstract 2511: New inhibitors the tyrosine kinase ACK1/TNK2 active in prostate, breast and pancreatic cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2511.

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Jin, Meizhong, Jing Wang, Andrew Kleinberg, Mridula Kadalbajoo, Kam W. Siu, Andrew Cooke, Mark Bittner, et al. "Abstract 2463: Discovery of imidazo[1,5-a]pyrazine derived potent, selective and orally bioavailable ACK1 inhibitors." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-2463.

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Olabisi, Oyenike, Vladyslav Kholodovych, Alam Nur-E. Kamal, Safirah Stewart-Singleton, Christina Andayah, Richard Wood, and William Welsh. "Abstract A13: Discovery of selective inhibitors of the kinase and metastatic activities of the activated Cdc42-associated kinase (ACK1)." In Abstracts: AACR International Conference on Translational Cancer Medicine-- Jul 11-14, 2010; San Francisco, CA. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1078-0432.tcmusa10-a13.

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Mahajan, Nupam, Kiran Mahajan, Harshani Lawrence, and Nicholas Lawrence. "Abstract A084: Reprogramming of androgen receptor gene expression by ACK1/TNK2 mediated histone H4 Tyr88-phosphorylation promotes castration resistance." In Abstracts: AACR Special Conference: Prostate Cancer: Advances in Basic, Translational, and Clinical Research; December 2-5, 2017; Orlando, Florida. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.prca2017-a084.

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Mahajan, Nupam P., Kiran Mahajan, Nicholas Lawrence, and Harshani Lawrence. "Abstract 2378: Histone H4 tyr88-phosphorylation mediated by ACK1 promotes castration-resistant prostate cancer by epigenetic reprogramming of androgen receptor." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-2378.

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Reports on the topic "Ack1"

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Stearns, Carrie. Role of the Non-Receptor Tyrosine Kinase ACK2 in EGF Receptor Degradation. Fort Belvoir, VA: Defense Technical Information Center, April 2004. http://dx.doi.org/10.21236/ada427754.

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Stearns, Carrie. Role of the Non-Receptor Tyrosine Kinase ACK2 in EGF Receptor Degradation. Fort Belvoir, VA: Defense Technical Information Center, April 2005. http://dx.doi.org/10.21236/ada435047.

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Rivera, Charlene. Role of Nonreceptor Protein Kinase Ack 1 in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2011. http://dx.doi.org/10.21236/ada545693.

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Kuzmanovic, A., A. Mondal, S. Floyd, and K. Ramakrishnan. Adding Explicit Congestion Notification (ECN) Capability to TCP's SYN/ACK Packets. RFC Editor, June 2009. http://dx.doi.org/10.17487/rfc5562.

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Modzelewska, Katarzyna. Ack-1 Tyrosine Kinase Regulates Integrin Signaling Leading to Breast Cell Migration. Fort Belvoir, VA: Defense Technical Information Center, March 2004. http://dx.doi.org/10.21236/ada426124.

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Modzelewska, Katarzyna, and Patricia J. Keely. Ack-1 Tyrosine Kinase Regulates Integrin Signaling Leading to Breast Cell Migration. Fort Belvoir, VA: Defense Technical Information Center, March 2003. http://dx.doi.org/10.21236/ada415773.

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Charles Kessel, et al. The Physics Basis For An Advanced Physics And Advanced Technology Tokamak Power Plant Configuration, ARIES-ACT1. Office of Scientific and Technical Information (OSTI), March 2014. http://dx.doi.org/10.2172/1128915.

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