IndraLab

"These findings provide valuable insights into the complex molecular interactions involved in tumor formation and highlight the potential of targeting the USP36-ALKBH5 axis as a therapeutic intervention for glioblastoma."

"Subsequent mass spectrometry experiments were conducted to unveil the protein interaction partners of ALKBH5, and the results demonstrated the interaction between USP36 and ALKBH5 [ xref ]."

"Another m 6 A modifier, ALKBH5, is stabilized by the deubiquitinase USP36 in GSCs, stimulating tumor growth and TMZ resistance [ xref ], and this USP36–ALKBH5 relationship may provide another targetable scaffold in GSCs."

"Mass spectrometry and immunoprecipitation were performed to identify the USP36 and ALKBH5 interaction."

"Our findings indicate that USP36 regulates the protein degradation and expression of ALKBH5, and the USP36-ALKBH5 axis orchestrates glioma tumorigenesis."

"Together, these findings underscore the crucial role of the USP36–ALKBH5 axis in governing GSC cell proliferation, stemness and tumorigenesis, and could potentially lay the groundwork for progressing the development of more potent therapies targeting glioblastoma [ xref , xref ]. xref illustrates the various regulators and mechanisms for dysregulation of m 6 A-related genes discussed in this sector."

"For example, the USP36–ALKBH5 axis has been shown to impart resistance to TMZ, the first-line chemotherapeutic agent for standard practice in the management of glioblastoma [ xref ]."

"ALKBH5 deficiency decreased PD‐L1 protein level by suppressing ZDHHC3 mRNA expression in an m 6 A modification manner, further enhancing the efficacy of anti‐PD‐1 therapy for GBM. xref ALKBH5 facilitates hypoxia‐induced paraspeckle assembly and IL8 secretion to recruit tumor‐associated macrophages (TAMs) to promote GBM progression. xref Ubiquitin‐specific peptidase 36 (USP36) interacts with and stabilizes ALKBH5, and targeting USP36‐ALKBH5 axis inhibits cell proliferation and self‐renewal of GSCs and sensitized GSCs to temozolomide (TMZ) treatment. xref It has been reported that ALKBH5 maintains tumorigenicity of GBM stem‐like cells (GSCs) by sustaining FOXM1 mRNA expression and cell proliferation program. xref We also found that ALKBH5 expression was associated with malignant proliferation of GBM and stemness of GSCs, but we focused on the alternative splicing events and isoform switch of target genes rather than mRNA expression."

"Subsequent studies have also found that ALKBH5 and USP36 interact to maintain stem cell properties in glioblastoma and promote tumor progression (Chang et al., 2023[ xref ])."

"Subsequent mass spectrometry experiments were conducted to unveil the protein interaction partners of ALKBH5, and the results demonstrated the interaction between USP36 and ALKBH5 [53]."

"For example, USP36 interacted with and stabilized ALKBH5 in glioblastoma [14]."

"Additionally, USP36 interacts with and upregulates ALKBH5, an m6A demethylase."