CoChat
Sign Up
Cited by 56

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Phosphorylation of the myosin IIA tailpiece regulates single myosin IIA molecule association with lytic granules to promote NK-cell cytotoxicity

Sanborn, Keri B., Mace, Emily M., Rak, Gregory D., Difeo, Analisa, Martignetti, John A., Pecci, Alessandro, Bussel, James B., Favier, Rémi, Orange, Jordan S.·2011·Blood
DOI 10.1182/blood-2011-03-344846
Open this paper in CoChat — free account

Abstract

Natural killer (NK) cells are innate immune lymphocytes that provide critical defense against virally infected and transformed cells. NK-cell cytotoxicity requires the formation of an F-actin rich immunologic synapse (IS), as well as the polarization of perforin-containing lytic granules to the IS and secretion of their contents at the IS. It was reported previously that NK-cell cytotoxicity requires nonmuscle myosin IIA function and that granule-associated myosin IIA mediates the interaction of granules with F-actin at the IS. In the present study, we evaluate the nature of the association of myosin IIA with lytic granules. Using NK cells from patients with mutations in myosin IIA, we found that the nonhelical tailpiece is required for NK-cell cytotoxicity and for the phosphorylation of granule-associated myosin IIA. Ultra-resolution imaging techniques demonstrated that single myosin IIA molecules associate with NK-cell lytic granules via the nonhelical tailpiece. Phosphorylation of myosin IIA at residue serine 1943 (S1943) in the tailpiece is needed for this linkage. This defines a novel mechanism for myosin II function, in which myosin IIA can act as a single-molecule actin motor, claiming granules as cargo through tail-dependent phosphorylation for the execution of a pre-final step in human NK-cell cytotoxicity.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1182/blood-2011-03-344846

Cites

1 of 1 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Show all 1 references

Research works printed but not linked: 48

  1. Orange, 2003, The mature activating natural killer cell immunologic synapse is formed in distinct stages., Proc Natl Acad Sci U S A, 100, 14151, 10.1073/pnas.1835830100 · DOI
  2. Mentlik, 2010, Rapid lytic granule convergence to the MTOC in natural killer cells is dependent on dynein but not cytolytic commitment., Mol Biol Cell, 21, 2241, 10.1091/mbc.e09-11-0930 · DOI
  3. Davis, 1999, The human natural killer cell immune synapse., Proc Natl Acad Sci U S A, 96, 15062, 10.1073/pnas.96.26.15062 · DOI
  4. Orange, 2008, Formation and function of the lytic NK-cell immunological synapse., Nat Rev Immunol, 8, 713, 10.1038/nri2381 · DOI
  5. Carpén, 1983, Polarization of NK cell cytoskeleton upon conjugation with sensitive target cells., J Immunol, 131, 2695, 10.4049/jimmunol.131.6.2695 · DOI
  6. Hoves, 2010, The battlefield of perforin/granzyme cell death pathways., J Leukoc Biol, 87, 237, 10.1189/jlb.0909608 · DOI
  7. Sanborn, 2010, Navigating barriers: the challenge of directed secretion at the natural killer cell lytic immunological synapse., J Clin Immunol, 30, 358, 10.1007/s10875-010-9372-y · DOI
  8. Jacobelli, 2004, A single class II myosin modulates T cell motility and stopping, but not synapse formation., Nat Immunol, 5, 531, 10.1038/ni1065 · DOI
  9. Andzelm, 2007, Myosin IIA is required for cytolytic granule exocytosis in human NK cells., J Exp Med, 204, 2285, 10.1084/jem.20071143 · DOI · Paper page
  10. Ludowyke, 2006, Phosphorylation of nonmuscle myosin heavy chain IIA on Ser1917 is mediated by protein kinase C beta II and coincides with the onset of stimulated degranulation of RBL-2H3 mast cells., J Immunol, 177, 1492, 10.4049/jimmunol.177.3.1492 · DOI
  11. Lee, 2004, Dictyostelium PAKc is required for proper chemotaxis., Mol Biol Cell, 15, 5456, 10.1091/mbc.e04-04-0323 · DOI
  12. Geisbrecht, 2002, Myosin VI is required for E-cadherin-mediated border cell migration., Nat Cell Biol, 4, 616, 10.1038/ncb830 · DOI
  13. Deng, 1999, A targeted gene silencing technique shows that Drosophila myosin VI is required for egg chamber and imaginal disc morphogenesis., J Cell Sci, 112, 3677, 10.1242/jcs.112.21.3677 · DOI
  14. Sanborn, 2009, Myosin IIA associates with NK cell lytic granules to enable their interaction with F-actin and function at the immunological synapse., J Immunol, 182, 6969, 10.4049/jimmunol.0804337 · DOI · Paper page
  15. Eddinger, 2007, Myosin II isoforms in smooth muscle: heterogeneity and function., Am J Physiol Cell Physiol, 293, C493, 10.1152/ajpcell.00131.2007 · DOI
  16. Ricketson, 2010, Multiple tail domain interactions stabilize nonmuscle myosin II bipolar filaments., Proc Natl Acad Sci U S A, 107, 20964, 10.1073/pnas.1007025107 · DOI
  17. Seri, 2003, MYH9-related disease: May-Hegglin anomaly, Sebastian syndrome, Fechtner syndrome, and Epstein syndrome are not distinct entities but represent a variable expression of a single illness., Medicine (Baltimore), 82, 203, 10.1097/01.md.0000076006.64510.5c · DOI
  18. Orange, 2002, Wiskott-Aldrich syndrome protein is required for NK cell cytotoxicity and colocalizes with actin to NK cell-activating immunologic synapses., Proc Natl Acad Sci U S A, 99, 11351, 10.1073/pnas.162376099 · DOI
  19. Heath, 2001, Nonmuscle myosin heavy chain IIA mutations define a spectrum of autosomal dominant macrothrombocytopenias: May-Hegglin anomaly and Fechtner, Sebastian, Epstein, and Alport-like syndromes., Am J Hum Genet, 69, 1033, 10.1086/324267 · DOI
  20. Banerjee, 2007, Cdc42-interacting protein-4 functionally links actin and microtubule networks at the cytolytic NK cell immunological synapse., J Exp Med, 204, 2305, 10.1084/jem.20061893 · DOI
  21. Orange, 2011, IL-2 induces a WAVE2-dependent pathway for actin reorganization that enables WASp-independent human NK cell function., J Clin Invest, 121, 1535, 10.1172/JCI44862 · DOI
  22. Kunishima, 2010, Advances in the understanding of MYH9 disorders., Curr Opin Hematol, 17, 405, 10.1097/MOH.0b013e32833c069c · DOI
  23. Dong, 2005, Genotype-phenotype correlation in MYH9-related thrombocytopenia., Br J Haematol, 130, 620, 10.1111/j.1365-2141.2005.05658.x · DOI
  24. Pecci, 2008, Position of nonmuscle myosin heavy chain IIA (NMMHC-IIA) mutations predicts the natural history of MYH9-related disease., Hum Mutat, 29, 409, 10.1002/humu.20661 · DOI
  25. Franke, 2005, Rod mutations associated with MYH9-related disorders disrupt nonmuscle myosin-IIA assembly., Blood, 105, 161, 10.1182/blood-2004-06-2067 · DOI
  26. Dulyaninova, 2005, Regulation of myosin-IIA assembly and Mts1 binding by heavy chain phosphorylation., Biochemistry, 44, 6867, 10.1021/bi0500776 · DOI
  27. Moussavi, 1993, Phosphorylation of vertebrate nonmuscle and smooth muscle myosin heavy chains and light chains., Mol Cell Biochem, 127–128, 219, 10.1007/BF01076773 · DOI
  28. Ronen, 2009, Myosin II tailpiece determines its paracrystal structure, filament assembly properties, and cellular localization., J Biol Chem, 284, 24948, 10.1074/jbc.M109.023754 · DOI
  29. Sandquist, 2008, The C-terminal tail region of nonmuscle myosin II directs isoform-specific distribution in migrating cells., Mol Biol Cell, 19, 5156, 10.1091/mbc.e08-05-0533 · DOI
  30. Kriajevska, 1998, Metastasis-associated Mts1 (S100A4) protein modulates protein kinase C phosphorylation of the heavy chain of nonmuscle myosin., J Biol Chem, 273, 9852, 10.1074/jbc.273.16.9852 · DOI
  31. Murakami, 1994, Direct binding of myosin II to phospholipid vesicles via tail regions and phosphorylation of the heavy chains by protein kinase C., J Biol Chem, 269, 16082, 10.1016/S0021-9258(17)33976-5 · DOI
  32. Fath, 2005, Characterization of myosin-II binding to Golgi stacks in vitro., Cell Motil Cytoskeleton, 60, 222, 10.1002/cm.20060 · DOI
  33. Kunishima, 2001, Identification of six novel MYH9 mutations and genotype-phenotype relationships in autosomal dominant macrothrombocytopenia with leukocyte inclusions., J Hum Genet, 46, 722, 10.1007/s100380170007 · DOI
  34. Conti, 1991, Identification of the serine residue phosphorylated by protein kinase C in vertebrate nonmuscle myosin heavy chains., Biochemistry, 30, 966, 10.1021/bi00218a012 · DOI
  35. Murakami, 1998, Two nonmuscle myosin II heavy chain isoforms expressed in rabbit brains: filament forming properties, the effects of phosphorylation by protein kinase C and casein kinase II, and location of the phosphorylation sites., Biochemistry, 37, 1989, 10.1021/bi971959a · DOI
  36. Akhmanova, 2010, Linking molecular motors to membrane cargo., Curr Opin Cell Biol, 22, 479, 10.1016/j.ceb.2010.04.008 · DOI
  37. Svitkina, 2009, Imaging cytoskeleton components by electron microscopy., Methods Mol Biol, 586, 187, 10.1007/978-1-60761-376-3_10 · DOI
  38. Huang, 2010, Breaking the diffraction barrier: super-resolution imaging of cells., Cell, 143, 1047, 10.1016/j.cell.2010.12.002 · DOI
  39. Straussman, 2005, Skip residues and charge interactions in myosin II coiled-coils: implications for molecular packing., J Mol Biol, 353, 613, 10.1016/j.jmb.2005.08.010 · DOI
  40. Kunishima, 2001, Mutations in the NMMHC-A gene cause autosomal dominant macrothrombocytopenia with leukocyte inclusions (May-Hegglin anomaly/Sebastian syndrome)., Blood, 97, 1147, 10.1182/blood.V97.4.1147 · DOI
  41. Müsch, 1997, Myosin II is involved in the production of constitutive transport vesicles from the TGN., J Cell Biol, 138, 291, 10.1083/jcb.138.2.291 · DOI
  42. Neco, 2004, New roles of myosin II during vesicle transport and fusion in chromaffin cells., J Biol Chem, 279, 27450, 10.1074/jbc.M311462200 · DOI
  43. Linz-McGillem, 2003, Myosin II in retinal pigmented epithelial cells: evidence for an association with membranous vesicles., Exp Eye Res, 76, 543, 10.1016/S0014-4835(03)00031-9 · DOI
  44. DePina, 2007, Membrane associated nonmuscle myosin II functions as a motor for actin-based vesicle transport in clam oocyte extracts., Cell Motil Cytoskeleton, 64, 739, 10.1002/cm.20219 · DOI
  45. Yu, 2007, Multiple myosins are required to coordinate actin assembly with coat compression during compensatory endocytosis., Mol Biol Cell, 18, 4096, 10.1091/mbc.e06-11-0993 · DOI
  46. Seabrooke, 2010, Nonmuscle myosin II helps regulate synaptic vesicle mobility at the Drosophila neuromuscular junction., BMC Neurosci, 11, 37, 10.1186/1471-2202-11-37 · DOI
  47. Norstrom, 2010, Unconventional processive mechanics of non-muscle myosin IIB., J Biol Chem, 285, 26326, 10.1074/jbc.M110.123851 · DOI
  48. Gross, 2007, Cargo transport: two motors are sometimes better than one., Curr Biol, 17, R478, 10.1016/j.cub.2007.04.025 · DOI

Cited by

See all 56

Metadata

Authors
Sanborn, K. B., Mace, E. M., Rak, G. D., Difeo, A., Martignetti, J. A., Pecci, A., Bussel, J. B., Favier, R., & Orange, J. S.
Affiliations
  • Immunology Graduate Group, University of Pennsylvania School of Medicine, Philadelphia, PA;
  • Children's Hospital Research Institute, Children's Hospital of Philadelphia, Philadelphia, PA;
  • Department of Genetics and Genomic Sciences, Mount Sinai School of Medicine, New York, NY;
  • Department of Internal Medicine, Istituto di Ricovero e Cura a Carattere Scientifico San Matteo, University of Pavia, Pavia, Italy;
  • Weill-Cornell Medical College of Cornell University, New York, NY; and
  • Assistance Publique–Hopitaux de Paris, Centre de Recherches en Physique des Plasmas, Armand Trousseau Children's Hospital, Villejuif, France
Venue
Blood
Publisher
American Society of Hematology
Published
2011-11-24
Volume
118
Issue
22
Pages
5862-5871
ISSN
  • 0006-4971
  • 1528-0020
DOI
10.1182/blood-2011-03-344846
Cited by
56
References
1
Language
en

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review

How to cite

Cite CoChat for the checks on this page, and the paper for its own findings.

This page
CoChat. (2026). Citation check: Phosphorylation of the myosin IIA tailpiece regulates single myosin IIA molecule association with lytic granules to promote NK-cell cytotoxicity. https://app.cochat.ai/papers/10.1182/blood-2011-03-344846
The paper
Sanborn, K. B., Mace, E. M., Rak, G. D., Difeo, A., Martignetti, J. A., Pecci, A., Bussel, J. B., Favier, R., & Orange, J. S. (2011). Phosphorylation of the myosin IIA tailpiece regulates single myosin IIA molecule association with lytic granules to promote NK-cell cytotoxicity. Blood. https://doi.org/10.1182/blood-2011-03-344846