ReviewInternational journal of general medicine2026
Dual Regulation of Post-Translational Modification of Proteins: Bottlenecks and Breakthroughs in NK Cell Therapy for Glioblastoma.
Review in International journal of general medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is the most malignant primary central nervous system tumor in adults, with strong invasiveness, high recurrence, and poor prognosis. Natural killer (NK) cells, innate immune cells that eliminate glioma stem cells without MHC matching, show promise for GBM immunotherapy, but their efficacy is limited by GBM's immunosuppressive tumor microenvironment (TME), especially via protein post-translational modifications (PTMs). This review summarizes seven key PTMs' (phosphorylation, acetylation, glycosylation, methylation, ubiquitination, SUMOylation, lactylation) dual regulation on NK cell therapy: physiological PTMs enhance NK cytotoxicity, targeting, and persistence; aberrant PTMs block NK activation, induce exhaustion, and promote GBM immune escape. It also analyzes bottlenecks (insufficient NK activity/persistence, GBM's PTM-mediated escape) and breakthroughs (PTM-targeted small molecules like TAK-981, CRISPR-edited NK cells, combination therapies). Future directions include BBB precision delivery, PTM-guided personalized therapy, and PTM crosstalk research, aiming to advance NK therapy's clinical translation for GBM.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.