2022
DOI: 10.1016/j.coi.2021.12.002
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Antibody glycosylation directs innate and adaptive immune collaboration

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Cited by 3 publications
(2 citation statements)
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“… 143 BMI-1-deficient mice showed engraftment and proliferative disability and stimulated differentiation and apoptosis in AML stem/progenitor cells. 144 , 145 BMI-1 and Ring1b can organize a heterodimeric complex that is involved in the initiation and maintenance of LSCs. Epigenetic inhibition of BMI-1, including methylation, histone deacetylase, and ubiquitin-proteasome could be utilized as anti-BMI-1 insights in LSCs.…”
Section: Signaling Pathways Governing Lsc Maintenancementioning
confidence: 99%
“… 143 BMI-1-deficient mice showed engraftment and proliferative disability and stimulated differentiation and apoptosis in AML stem/progenitor cells. 144 , 145 BMI-1 and Ring1b can organize a heterodimeric complex that is involved in the initiation and maintenance of LSCs. Epigenetic inhibition of BMI-1, including methylation, histone deacetylase, and ubiquitin-proteasome could be utilized as anti-BMI-1 insights in LSCs.…”
Section: Signaling Pathways Governing Lsc Maintenancementioning
confidence: 99%
“…Also, these changes of glycosylation also cause abnormal expression of membrane-localized glycans, which will trigger cellular malignant transformation and mediate cancer cell proliferation, survival, and metastasis ( Marsico et al, 2018 ; Chandler et al, 2019 ; Thomas et al, 2021 ). Accumulating findings suggest that abnormal glycan profiles could regulate the microenvironment and immune response ( Mereiter et al, 2019 ) and even hinder an effective immune response ( Polmear and Good-Jacobson, 2021 ). In addition, the metabolic state ( Campbell and Wellen, 2018 ) or metabolic reprogramming ( Carvalho-Cruz et al, 2018 ) of the tumor cell can lead to aberrant glycosylation intra- and extra-cellular.…”
Section: Introductionmentioning
confidence: 99%