SHIP-1 deficiency in the myeloid compartment is insufficient to induce myeloid expansion or chronic inflammation. (Q53292640)

13 May 2018

title

SHIP-1 deficiency in the myeloid compartment is insufficient to induce myeloid expansion or chronic inflammation. (English)

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13 May 2018

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6

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author name string

M J Maxwell

1

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13 May 2018

N Srivastava

2

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M-Y Park

3

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13 May 2018

E Tsantikos

4

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R W Engelman

5

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13 May 2018

M L Hibbs

7

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13 May 2018

publication date

6 March 2014

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13 May 2018

published in

Genes and Immunity

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13 May 2018

volume

15

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13 May 2018

issue

4

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page(s)

233-240

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https://scigraph.springernature.com/pub.10.1038/gene.2014.9

exact match

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cites work

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Taming the PI3K team to hold inflammation and cancer at bay.

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Inhibitor and activator: dual functions for SHIP in immunity and cancer

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Targeting of the GTPase Irgm1 to the phagosomal membrane via PtdIns(3,4)P(2) and PtdIns(3,4,5)P(3) promotes immunity to mycobacteria

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SHIP1 inhibition increases immunoregulatory capacity and triggers apoptosis of hematopoietic cancer cells.

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Targeted disruption of SHIP leads to hemopoietic perturbations, lung pathology, and a shortened life span

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SHIP is a negative regulator of growth factor receptor-mediated PKB/Akt activation and myeloid cell survival

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Perturbed myelo/erythropoiesis in Lyn-deficient mice is similar to that in mice lacking the inhibitory phosphatases SHP-1 and SHIP-1.

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Genetic segregation of inflammatory lung disease and autoimmune disease severity in SHIP-1-/- mice

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SHIP represses the generation of alternatively activated macrophages

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M-1/M-2 macrophages and the Th1/Th2 paradigm

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SHIP deficiency causes Crohn's disease-like ileitis

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SHIP-deficient mice develop spontaneous intestinal inflammation and arginase-dependent fibrosis

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Macrophages control the retention and trafficking of B lymphocytes in the splenic marginal zone

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Lineage extrinsic and intrinsic control of immunoregulatory cell numbers by SHIP.

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Conditional gene targeting in macrophages and granulocytes using LysMcre mice.

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An ENU-induced mouse mutant of SHIP1 reveals a critical role of the stem cell isoform for suppression of macrophage activation.

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Marginal zone B cells exhibit unique activation, proliferative and immunoglobulin secretory responses.

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The inositol polyphosphate 5-phosphatase ship is a crucial negative regulator of B cell antigen receptor signaling

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SHIP-deficient mice are severely osteoporotic due to increased numbers of hyper-resorptive osteoclasts

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The src homology 2-containing inositol phosphatase (SHIP) is the gatekeeper of mast cell degranulation

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SHIP1 and Lyn Kinase Negatively Regulate Integrin alpha IIb beta 3 signaling in platelets.

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Cutting edge: dominance by an MHC-independent inhibitory receptor compromises NK killing of complex targets

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Src homology 2 domain-containing inositol 5-phosphatase 1 deficiency leads to a spontaneous allergic inflammation in the murine lung

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The inositol 5'-phosphatase SHIP-1 and the Src kinase Lyn negatively regulate macrophage colony-stimulating factor-induced Akt activity

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SHIP represses the generation of IL-3-induced M2 macrophages by inhibiting IL-4 production from basophils.

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Inhibition of the immunosuppressive activity of resident pulmonary alveolar macrophages by granulocyte/macrophage colony-stimulating factor

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Transplantable myeloproliferative disease induced in mice by an interleukin 6 retrovirus

21 January 2018

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IL-6 blocks a discrete early step in lymphopoiesis

21 January 2018

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Interleukin 6 enhancement of interleukin 3-dependent proliferation of multipotential hemopoietic progenitors

21 January 2018

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Src homology 2-containing 5-inositol phosphatase (SHIP) suppresses an early stage of lymphoid cell development through elevated interleukin-6 production by myeloid cells in bone marrow

21 January 2018

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SHIP is required for a functional hematopoietic stem cell niche.

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Many mechanisms mediating mobilization: an alliterative review

21 January 2018

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SHIP deficiency enhances HSC proliferation and survival but compromises homing and repopulation

21 January 2018

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Embryonic and hematopoietic stem cells express a novel SH2-containing inositol 5'-phosphatase isoform that partners with the Grb2 adapter protein

21 January 2018

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T cell-specific deletion of the inositol phosphatase SHIP reveals its role in regulating Th1/Th2 and cytotoxic responses

21 January 2018

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Recipient CD4+ T cells that survive irradiation regulate chronic graft-versus-host disease

21 January 2018

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Influence of SHIP on the NK Repertoire and Allogeneic Bone Marrow Transplantation

21 January 2018

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https://api.crossref.org/works/10.1038%2FGENE.2014.9

21 January 2018

12 December 2020

Myeloid cell-specific expression of Ship1 regulates IL-12 production and immunity to helminth infection

1 reference

https://api.crossref.org/works/10.1038%2FGENE.2014.9

LPS-Induced Upregulation of SHIP Is Essential for Endotoxin Tolerance

21 January 2018

1 reference

12 December 2020

Enhancement of murine hematopoiesis by synergistic interactions between steel factor (ligand for c-kit), interleukin-11, and other early acting factors in culture

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12 December 2020

Expansion of myeloid suppressor cells in SHIP-deficient mice represses allogeneic T cell responses

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12 December 2020

A dual role for Src homology 2 domain-containing inositol-5-phosphatase (SHIP) in immunity: aberrant development and enhanced function of b lymphocytes in ship -/- mice

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12 December 2020

Distinct macrophage subpopulations characterize acute infection and chronic inflammatory lung disease

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12 December 2020

Rat tracheal epithelial cells produce granulocyte/macrophage colony-stimulating factor

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12 December 2020

Identifiers

DOI

10.1038/GENE.2014.9

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13 May 2018

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13 May 2018