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Article: Safety of Repeated Administration of Xenogeneic Human Apoptotic State (Allocetra-OTS) in Sprague Dawley Rats.

Ankri, Chen / Hershkovitz, Oren / Hershkovitz, Liat / Brami, Meital / Levy, Ronnie / Sarig, Hadar / Souli, Einat / Reicher, Barak / Amor-Baroukh, Veronique / Mevorach, Dror / Nyska, Abraham

Pharmaceutics

2024 Volume 16, Issue 3

Abstract: Apoptotic cells possess immunomodulatory effects that can be utilized to treat imbalanced immune conditions. Information on the preclinical safety of such treatment is sparse. In this study, the safety of apoptotic cells (Allocetra-OTS) was assessed in a ...

Abstract	Apoptotic cells possess immunomodulatory effects that can be utilized to treat imbalanced immune conditions. Information on the preclinical safety of such treatment is sparse. In this study, the safety of apoptotic cells (Allocetra-OTS) was assessed in a GLP toxicological study on Sprague Dawley rats. Three doses of Allocetra-OTS or vehicle were administered intravenously (IV) for 3 consecutive days. Animals in the main study were sacrificed on day 4, while animals from the recovery groups were kept for 14 or 28 days. Allocetra-OTS was well tolerated, and no adverse effects were observed in terms of body weight, clinical signs, food consumption, or ophthalmologic observation. Thus, the No Observed Adverse Effect Level (NOAEL) dose was determined as the highest dose administered. An observed elevation in immune cells was suspected to be due to Allocetra-OTS, similarly to other clinical chemistry parameters; however, it was resolved in the recovery phases. Splenomegaly and dose-related extramedullary hematopoiesis (EMH) in the red pulp were observed, with no adverse events, and were considered to be a normal and expected reaction following the IV administration of cell-based therapies. In conclusion, under the conditions of this study, Allocetra-OTS was concluded to be safe, further supporting its potential candidacy for clinical studies.
Language	English
Publishing date	2024-03-20
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527217-2
ISSN	1999-4923
ISSN	1999-4923
DOI	10.3390/pharmaceutics16030426
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Article ; Online: Apoptotic cells for treatment of acute respiratory distress syndrome associated with COVID-19.

van Heerden, Peter Vernon / Abutbul, Avraham / Naama, Ahmad / Maayan, Shlomo / Makram, Nassar / Nachshon, Akiva / Abu Jabal, Kamal / Hershkovitz, Oren / Binder, Lior / Shabat, Yehudit / Reicher, Barak / Mevorach, Dror

Frontiers in immunology

2023 Volume 14, Page(s) 1242551

Abstract: Background: Hyper-inflammatory immune response, a hallmark of severe COVID-19, is associated with increased mortality. Acute respiratory distress syndrome (ARDS) is a common manifestation. We undertook two phase I/II studies in five and then 16 subjects ...

Abstract	Background: Hyper-inflammatory immune response, a hallmark of severe COVID-19, is associated with increased mortality. Acute respiratory distress syndrome (ARDS) is a common manifestation. We undertook two phase I/II studies in five and then 16 subjects with severe/critical COVID-19 to assess the safety and preliminary efficacy of apoptotic cells (Allocetra™-OTS, Enlivex Therapeutics), a cellular immunomodulatory therapy that reprograms macrophages to reduce hyper-inflammatory response severity. Methods: Eligible patients presenting to the Emergency Room with severe COVID-19 and respiratory dysfunction received one intravenous administration of Allocetra™-OTS and were monitored for adverse events (AEs) for 28 days. The primary aim was to determine the safety profile of treatment; secondary aims were recovery from ARDS, intensive care unit (ICU) and hospital length-of-stay, and mortality. Immune modulator markers were measured to elucidate the mechanism of action of Allocetra™-OTS. Results: 21 patients with severe-critical COVID-19 of Gamma, Alpha and Delta variants, were treated with a single dose of apoptotic cells. 19/21 patients had mild-to-severe ARDS at presentation. Median age was 53 years, 16/21 were males, 16/21 were overweight/obese. No serious related adverse events (SAEs) were reported. All 21 study subjects survived to day 28 (end of study); 19/21 recovered completely. Comparable mortality rates at the hospital were 3.8%-8.9% for age- and gender-matched patients, and 39%-55% for critical patients. Recovering patients exhibited rapid ARDS resolution and parallel resolution of inflammation markers and elevated cytokines/chemokines. Conclusion: In patients with severe/critical COVID-19 associated with ARDS, Allocetra™-OTS was safe, well-tolerated, and showed promising results for resolution of respiratory failure and inflammation. Trial registration: https://clinicaltrials.gov/ct2/show/study/NCT04513470, https://clinicaltrials.gov/ct2/show/study/NCT04590053, Identifiers NCT04513470, NCT04590053.
MeSH term(s)	Male ; Humans ; Middle Aged ; Female ; COVID-19/complications ; SARS-CoV-2 ; Respiratory Distress Syndrome ; Inflammation ; Apoptosis
Language	English
Publishing date	2023-08-02
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1242551
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Article ; Online: Apoptotic cell therapy for cytokine storm associated with acute severe sepsis.

Karbian, Netanel / Abutbul, Avraham / El-Amore, Raja / Eliaz, Ran / Beeri, Ronen / Reicher, Barak / Mevorach, Dror

Cell death & disease

2020 Volume 11, Issue 7, Page(s) 535

Abstract: Sepsis has no proven pharmacologic treatment other than appropriate antibiotic agents, fluids, vasopressors as needed, and possibly corticosteroids. It is generally initiated mainly by the simultaneous recognition by various components of the innate ... ...

Abstract	Sepsis has no proven pharmacologic treatment other than appropriate antibiotic agents, fluids, vasopressors as needed, and possibly corticosteroids. It is generally initiated mainly by the simultaneous recognition by various components of the innate immune system of either pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs). In the current study, we employed the murine cecal ligation and puncture (CLP) model for sepsis to evaluate the effect of post-CLP infusion of apoptotic cells (Allocetra-OTS) on a CLP severe sepsis model. Cardiovascular evaluation, acute kidney injury (AKI), acute liver injury (ALI), and hematological and metabolic function were evaluated. Cytokine and chemokine profiles were measured by Multiplex ELISA and mitochondrial function, and glycolysis by Seahorse. The Murine Sepsis Score (MSS) was used for disease severity definition. CLP mice had low blood pressure, poor cardiac output, and lung dysfunction, as well as AKI, ALI, and thrombocytopenia, which correlated with the MSS and corresponded to a cytokine/chemokine storm. Apoptotic cell administration markedly improved the cytokine and chemokine storm and restored the impaired mitochondrial and glycolytic function in white blood cells leading to increased survival, from 6 to 60% (P < 0.0001), together with a significant improvement in organ dysfunction. We conclude that the deleterious immune response in CLP-induced sepsis can be successfully modified by apoptotic cell infusion.
MeSH term(s)	Animals ; Apoptosis ; Cytokine Release Syndrome/complications ; Disease Models, Animal ; Male ; Mice ; Sepsis/genetics ; Sepsis/pathology
Language	English
Publishing date	2020-07-15
Publishing country	England
Document type	Journal Article
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-020-02748-8
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Article ; Online: Multiple pathways leading from the T-cell antigen receptor to the actin cytoskeleton network.

Reicher, Barak / Barda-Saad, Mira

FEBS letters

2010 Volume 584, Issue 24, Page(s) 4858–4864

Abstract: Dynamic rearrangements of the actin cytoskeleton, following T-cell antigen receptor (TCR) engagement, provide the structural matrix and flexibility to enable intracellular signal transduction, cellular and subcellular remodeling, and driving effector ... ...

Abstract	Dynamic rearrangements of the actin cytoskeleton, following T-cell antigen receptor (TCR) engagement, provide the structural matrix and flexibility to enable intracellular signal transduction, cellular and subcellular remodeling, and driving effector functions. Recently developed cutting-edge imaging technologies have facilitated the study of TCR signaling and its role in actin-dependent processes. In this review, we describe how TCR signaling cascades induce the activation of actin regulatory proteins and the formation of actin networks, and how actin dynamics is important for T-cell homeostasis, activation, migration, and other effector functions.
MeSH term(s)	Actins/metabolism ; Animals ; Cytoskeleton/metabolism ; Humans ; Receptors, Antigen, T-Cell/metabolism ; Signal Transduction
Chemical Substances	Actins ; Receptors, Antigen, T-Cell
Language	English
Publishing date	2010-12-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1016/j.febslet.2010.09.002
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Article ; Online: Apoptotic Cells for Therapeutic Use in Cytokine Storm Associated With Sepsis- A Phase Ib Clinical Trial.

van Heerden, Peter Vernon / Abutbul, Avraham / Sviri, Sigal / Zlotnick, Eitan / Nama, Ahmad / Zimro, Sebastian / El-Amore, Raja / Shabat, Yehudit / Reicher, Barak / Falah, Batla / Mevorach, Dror

Frontiers in immunology

2021 Volume 12, Page(s) 718191

Abstract: Background: Sepsis has no proven specific pharmacologic treatment and reported mortality ranges from 30%-45%. The primary aim of this phase IB study was to determine the safety profile of Allocetra™-OTS (early apoptotic cell) infusion in subjects ... ...

Abstract	Background: Sepsis has no proven specific pharmacologic treatment and reported mortality ranges from 30%-45%. The primary aim of this phase IB study was to determine the safety profile of Allocetra™-OTS (early apoptotic cell) infusion in subjects presenting to the emergency room with sepsis. The secondary aims were to measure organ dysfunction, intensive care unit (ICU) and hospital stays, and mortality. Exploratory endpoints included measuring immune modulator agents to elucidate the mechanism of action. Methods: Ten patients presenting to the emergency room at the Hadassah Medical Center with sepsis were enrolled in this phase Ib clinical study. Enrolled patients were males and females aged 51-83 years, who had a Sequential Organ Failure Assessment (SOFA) score ≥2 above baseline and were septic due to presumed infection. Allocetra™-OTS was administered as a single dose (day +1) or in two doses of 140×10 Results: All 10 patients had mild-to-moderate sepsis with SOFA scores ranging from 2-6 upon entering the study. No SAEs and no related AEs were reported. All 10 study subjects survived, while matched historical controls had a mortality rate of 27%. The study subjects exhibited rapid resolution of organ dysfunction and had significantly shorter ICU stays compared to matched historical controls (p<0.0001). All patients had both elevated pro- and anti-inflammatory cytokines, chemokines, and additional immune modulators that gradually decreased following treatment. Conclusion: Administration of apoptotic cells to patients with mild-to-moderate sepsis was safe and had a significant immuno-modulating effect, leading to early resolution of the cytokine storm. Clinical trial registration: ClinicalTrials.gov Identifier: NCT03925857. (https://clinicaltrials.gov/ct2/show/study/NCT03925857).
MeSH term(s)	Aged ; Aged, 80 and over ; Apoptosis ; Autoantibodies ; Autoimmunity ; Biomarkers ; Cell- and Tissue-Based Therapy/adverse effects ; Cell- and Tissue-Based Therapy/methods ; Cytokine Release Syndrome/blood ; Cytokine Release Syndrome/complications ; Cytokine Release Syndrome/diagnosis ; Cytokine Release Syndrome/therapy ; Disease Management ; Disease Susceptibility ; Female ; Humans ; Immunologic Factors ; Male ; Middle Aged ; Organ Dysfunction Scores ; Sepsis/blood ; Sepsis/complications ; Sepsis/diagnosis ; Sepsis/therapy ; Treatment Outcome
Chemical Substances	Autoantibodies ; Biomarkers ; Immunologic Factors
Language	English
Publishing date	2021-09-30
Publishing country	Switzerland
Document type	Clinical Trial, Phase I ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.718191
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Article: The calcium feedback loop and T cell activation: how cytoskeleton networks control intracellular calcium flux.

Joseph, Noah / Reicher, Barak / Barda-Saad, Mira

Biochimica et biophysica acta

2014 Volume 1838, Issue 2, Page(s) 557–568

Abstract: During T cell activation, the engagement of a T cell with an antigen-presenting cell (APC) results in rapid cytoskeletal rearrangements and a dramatic increase of intracellular calcium (Ca(2+)) concentration, downstream to T cell antigen receptor (TCR) ... ...

Abstract	During T cell activation, the engagement of a T cell with an antigen-presenting cell (APC) results in rapid cytoskeletal rearrangements and a dramatic increase of intracellular calcium (Ca(2+)) concentration, downstream to T cell antigen receptor (TCR) ligation. These events facilitate the organization of an immunological synapse (IS), which supports the redistribution of receptors, signaling molecules and organelles towards the T cell-APC interface to induce downstream signaling events, ultimately supporting T cell effector functions. Thus, Ca(2+) signaling and cytoskeleton rearrangements are essential for T cell activation and T cell-dependent immune response. Rapid release of Ca(2+) from intracellular stores, e.g. the endoplasmic reticulum (ER), triggers the opening of Ca(2+) release-activated Ca(2+) (CRAC) channels, residing in the plasma membrane. These channels facilitate a sustained influx of extracellular Ca(2+) across the plasma membrane in a process termed store-operated Ca(2+) entry (SOCE). Because CRAC channels are themselves inhibited by Ca(2+) ions, additional factors are suggested to enable the sustained Ca(2+) influx required for T cell function. Among these factors, we focus here on the contribution of the actin and microtubule cytoskeleton. The TCR-mediated increase in intracellular Ca(2+) evokes a rapid cytoskeleton-dependent polarization, which involves actin cytoskeleton rearrangements and microtubule-organizing center (MTOC) reorientation. Here, we review the molecular mechanisms of Ca(2+) flux and cytoskeletal rearrangements, and further describe the way by which the cytoskeletal networks feedback to Ca(2+) signaling by controlling the spatial and temporal distribution of Ca(2+) sources and sinks, modulating TCR-dependent Ca(2+) signals, which are required for an appropriate T cell response. This article is part of a Special Issue entitled: Reciprocal influences between cell cytoskeleton and membrane channels, receptors and transporters. Guest Editor: Jean Claude Hervé.
MeSH term(s)	Animals ; Calcium/metabolism ; Calcium Signaling ; Cytoskeleton/metabolism ; Humans ; Lymphocyte Activation ; Signal Transduction ; T-Lymphocytes/metabolism
Chemical Substances	Calcium (SY7Q814VUP)
Language	English
Publishing date	2014-02
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbamem.2013.07.009
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Article ; Online: Wiskott-Aldrich syndrome protein--dynamic regulation of actin homeostasis: from activation through function and signal termination in T lymphocytes.

Matalon, Omri / Reicher, Barak / Barda-Saad, Mira

Immunological reviews

2013 Volume 256, Issue 1, Page(s) 10–29

Abstract: The actin cytoskeleton network forms a key link between T-cell antigen receptor (TCR) stimulation and T-cell effector functions, providing a structural basis for T-cell morphological changes and signal transduction. Accumulating evidence positions the ... ...

Abstract	The actin cytoskeleton network forms a key link between T-cell antigen receptor (TCR) stimulation and T-cell effector functions, providing a structural basis for T-cell morphological changes and signal transduction. Accumulating evidence positions the Wiskott-Aldrich syndrome protein (WASp), a scaffolding protein that promotes actin polymerization, at the center of actin cytoskeleton-dependent T-cell function. During the past decade, we and others have utilized multidisciplinary technologies, including live-cell imaging, biochemical, and biophysical analyses, to gain insight into the mechanisms by which WASp and other cytoskeletal proteins control actin homeostasis. Following TCR engagement, WASp is rapidly activated and recruited to TCR microclusters, as part of multiprotein complexes, where it promotes actin remodeling. Late in the activation process, WASp is internalized and eventually degraded. In this review, we describe the dynamic interactions of WASp with signaling proteins, which regulate its activation and recruitment to the TCR and to actin-rich sites. Finally, we present the molecular mechanism of WASp downregulation. Some of the signaling proteins that mediate WASp activation eventually lead to its degradation. Thus, we focus here on the regulation of WASp expression and function and the mechanisms whereby they control actin machinery and T-cell effector functions.
MeSH term(s)	Actins/metabolism ; Animals ; Homeostasis ; Humans ; Immunological Synapses/immunology ; Immunological Synapses/metabolism ; Protein Binding ; Protein Transport ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; Wiskott-Aldrich Syndrome Protein/chemistry ; Wiskott-Aldrich Syndrome Protein/metabolism
Chemical Substances	Actins ; Wiskott-Aldrich Syndrome Protein
Language	English
Publishing date	2013-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	391796-4
ISSN	1600-065X ; 0105-2896
ISSN (online)	1600-065X
ISSN	0105-2896
DOI	10.1111/imr.12112
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Article ; Online: A conformational change within the WAVE2 complex regulates its degradation following cellular activation.

Joseph, Noah / Biber, Guy / Fried, Sophia / Reicher, Barak / Levy, Omer / Sabag, Batel / Noy, Elad / Barda-Saad, Mira

Scientific reports

2017 Volume 7, Page(s) 44863

Abstract: WASp family Verprolin-homologous protein-2 (WAVE2), a member of the Wiskott-Aldrich syndrome protein (WASp) family of actin nucleation promoting factors, is a central regulator of actin cytoskeleton polymerization and dynamics. Multiple signaling ... ...

Abstract	WASp family Verprolin-homologous protein-2 (WAVE2), a member of the Wiskott-Aldrich syndrome protein (WASp) family of actin nucleation promoting factors, is a central regulator of actin cytoskeleton polymerization and dynamics. Multiple signaling pathways operate via WAVE2 to promote the actin-nucleating activity of the actin-related protein 2/3 (Arp2/3) complex. WAVE2 exists as a part of a pentameric protein complex known as the WAVE regulatory complex (WRC), which is unstable in the absence of its individual proteins. While the involvement of WAVE2 in actin polymerization has been well documented, its negative regulation mechanism is poorly characterized to date. Here, we demonstrate that WAVE2 undergoes ubiquitylation in a T-cell activation dependent manner, followed by proteasomal degradation. The WAVE2 ubiquitylation site was mapped to lysine 45, located at the N-terminus where WAVE2 binds to the WRC. Using Förster resonance energy transfer (FRET), we reveal that the autoinhibitory conformation of the WRC maintains the stability of WAVE2 in resting cells; the release of autoinhibition following T-cell activation facilitates the exposure of WAVE2 to ubiquitylation, leading to its degradation. The dynamic conformational structures of WAVE2 during cellular activation dictate its degradation.
MeSH term(s)	Amino Acids/metabolism ; Cell Line ; Humans ; Lymphocyte Activation/immunology ; Multiprotein Complexes/chemistry ; Multiprotein Complexes/metabolism ; Phosphorylation ; Protein Binding ; Protein Conformation ; Protein Interaction Domains and Motifs ; Protein Stability ; Proteolysis ; Receptors, Antigen, T-Cell/metabolism ; Structure-Activity Relationship ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; Ubiquitination ; Wiskott-Aldrich Syndrome Protein Family/chemistry ; Wiskott-Aldrich Syndrome Protein Family/genetics ; Wiskott-Aldrich Syndrome Protein Family/metabolism
Chemical Substances	Amino Acids ; Multiprotein Complexes ; Receptors, Antigen, T-Cell ; WASF2 protein, human ; Wiskott-Aldrich Syndrome Protein Family
Language	English
Publishing date	2017-03-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/srep44863
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Article ; Online: Ubiquitylation-dependent downregulation of Nck regulates its functional activity.

Joseph, Noah / Reicher, Barak / David, Ahuvit / Matalon, Omri / Barda-Saad, Mira

FEBS letters

2014 Volume 588, Issue 21, Page(s) 3808–3815

Abstract: The Nck adapter protein is involved in key cellular functions, such as actin polymerization and reorganization, serving as a molecular bridge between the surface complex essential for foreign antigen recognition, the T-cell antigen receptor (TCR), and ... ...

Abstract	The Nck adapter protein is involved in key cellular functions, such as actin polymerization and reorganization, serving as a molecular bridge between the surface complex essential for foreign antigen recognition, the T-cell antigen receptor (TCR), and the actin machinery. However, the mechanisms regulating Nck expression and functions are unknown. In this study, we revealed Nck negative regulation and demonstrated that Nck is ubiquitylated following cellular activation. We identified the molecular determinants and mediators involved in this process. Our data suggest that Nck ubiquitylation might serve as a mechanism controlling Nck-mediated effector functions during cellular activation.
MeSH term(s)	Actins/metabolism ; Adaptor Proteins, Signal Transducing/chemistry ; Adaptor Proteins, Signal Transducing/deficiency ; Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Cell Adhesion ; Down-Regulation ; Gene Silencing ; HEK293 Cells ; Humans ; Jurkat Cells ; Mutation ; Oncogene Proteins/chemistry ; Oncogene Proteins/deficiency ; Oncogene Proteins/genetics ; Oncogene Proteins/metabolism ; Proteasome Endopeptidase Complex/metabolism ; Proteolysis ; Proto-Oncogene Proteins c-cbl/metabolism ; RNA, Small Interfering/genetics ; Receptors, Antigen, T-Cell/metabolism ; Ubiquitination ; src Homology Domains
Chemical Substances	Actins ; Adaptor Proteins, Signal Transducing ; Nck protein ; Oncogene Proteins ; RNA, Small Interfering ; Receptors, Antigen, T-Cell ; Proto-Oncogene Proteins c-cbl (EC 2.3.2.27) ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
Language	English
Publishing date	2014-11-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1016/j.febslet.2014.08.033
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Article: Ubiquitylation-dependent downregulation of Nck regulates its functional activity

Joseph, Noah / Barak Reicher / Ahuvit David / Omri Matalon / Mira Barda-Saad

Federation of European Biochemical Societies FEBS letters. 2014 Nov. 03, v. 588, no. 21

2014

Abstract	The Nck adapter protein is involved in key cellular functions, such as actin polymerization and reorganization, serving as a molecular bridge between the surface complex essential for foreign antigen recognition, the T-cell antigen receptor (TCR), and the actin machinery. However, the mechanisms regulating Nck expression and functions are unknown. In this study, we revealed Nck negative regulation and demonstrated that Nck is ubiquitylated following cellular activation. We identified the molecular determinants and mediators involved in this process. Our data suggest that Nck ubiquitylation might serve as a mechanism controlling Nck-mediated effector functions during cellular activation.
Keywords	T-lymphocytes ; actin ; antigens ; polymerization
Language	English
Dates of publication	2014-1103
Size	p. 3808-3815.
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1016/j.febslet.2014.08.033
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