Isha Mondal
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View article: Mitochondrial stress-induced protein carboxyl-terminal alanine threonine tailing (msiCAT-tailing) facilitates glioblastoma tumorigenesis through the modulation of mitochondrial functions
Mitochondrial stress-induced protein carboxyl-terminal alanine threonine tailing (msiCAT-tailing) facilitates glioblastoma tumorigenesis through the modulation of mitochondrial functions Open
The rapid and sustained proliferation of cancer cells necessitates increased protein production, which, along with their disrupted metabolism, elevates the likelihood of translation errors. Ribosome-associated quality control (RQC), a rece…
View article: Supplementary Data from PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING-Type I Interferon Signaling in Glioblastoma
Supplementary Data from PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING-Type I Interferon Signaling in Glioblastoma Open
Supplementary Text Figs. S1 to S8 Tables S1 to S3
View article: Supplementary Data from PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING-Type I Interferon Signaling in Glioblastoma
Supplementary Data from PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING-Type I Interferon Signaling in Glioblastoma Open
Supplementary Text Figs. S1 to S8 Tables S1 to S3
View article: Supplementary Data from PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING-Type I Interferon Signaling in Glioblastoma
Supplementary Data from PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING-Type I Interferon Signaling in Glioblastoma Open
Cluster defining genes from scRNAseq data
View article: Supplementary Data from PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING-Type I Interferon Signaling in Glioblastoma
Supplementary Data from PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING-Type I Interferon Signaling in Glioblastoma Open
Cluster defining genes from scRNAseq data
View article: Data from PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING-Type I Interferon Signaling in Glioblastoma
Data from PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING-Type I Interferon Signaling in Glioblastoma Open
Glioblastoma (GBM) is an immunologically “cold” tumor that does not respond to current immunotherapy. Here, we demonstrate a fundamental role for the α-isoform of the catalytic subunit of protein phosphatase-2A (PP2Ac) in regulating glioma…
View article: The mitochondrial stress-induced protein carboxyl-terminal alanine and threonine tailing (msiCAT-tailing) promotes glioblastoma tumorigenesis by modulating mitochondrial functions
The mitochondrial stress-induced protein carboxyl-terminal alanine and threonine tailing (msiCAT-tailing) promotes glioblastoma tumorigenesis by modulating mitochondrial functions Open
The rapid and sustained proliferation in cancer cells requires accelerated protein synthesis. Accelerated protein synthesis and disordered cell metabolism in cancer cells greatly increase the risk of translation errors. ribosome-associated…
View article: Mitochondrial Protein Carboxyl-Terminal Alanine-Threonine Tailing Promotes Glioblastoma Tumor Growth by Regulating Mitochondrial Function
Mitochondrial Protein Carboxyl-Terminal Alanine-Threonine Tailing Promotes Glioblastoma Tumor Growth by Regulating Mitochondrial Function Open
The rapid and sustained proliferation of cancer cells necessitates increased protein production, which, along with their disrupted metabolism, elevates the likelihood of translation errors. Ribosome-associated quality control (RQC), a rece…
View article: Mitochondrial Protein Carboxyl-Terminal Alanine-Threonine Tailing Promotes Glioblastoma Tumor Growth by Regulating Mitochondrial Function
Mitochondrial Protein Carboxyl-Terminal Alanine-Threonine Tailing Promotes Glioblastoma Tumor Growth by Regulating Mitochondrial Function Open
The rapid and sustained proliferation of cancer cells necessitates increased protein production, which, along with their disrupted metabolism, elevates the likelihood of translation errors. Ribosome-associated quality control (RQC), a rece…
View article: Glioma–Immune Cell Crosstalk in Tumor Progression
Glioma–Immune Cell Crosstalk in Tumor Progression Open
Glioma progression is a complex process controlled by molecular factors that coordinate the crosstalk between tumor cells and components of the tumor microenvironment (TME). Among these, immune cells play a critical role in cancer survival…
View article: CCRG-06. PP2A DEFICIENCY INDUCES CELLULAR SENESCENCE AND SENSITIZES P53 MUTANT TUMORS TO SENOLYTIC THERAPY
CCRG-06. PP2A DEFICIENCY INDUCES CELLULAR SENESCENCE AND SENSITIZES P53 MUTANT TUMORS TO SENOLYTIC THERAPY Open
Loss of p53 can promote tumor progression by preventing induction of senescence, a critical tumor-suppressive mechanism that limits tumor proliferation. Promotion of senescence in a p53-independent manner can be a novel strategy to overcom…
View article: TMIC-65. PP2A/STRN4 NEGATIVELY REGULATES STING-TYPE I IFN SIGNALING IN GLIOMA ASSOCIATED MACROPHAGES THROUGH YAP/TAZ
TMIC-65. PP2A/STRN4 NEGATIVELY REGULATES STING-TYPE I IFN SIGNALING IN GLIOMA ASSOCIATED MACROPHAGES THROUGH YAP/TAZ Open
Glioma associated Macrophages/microglia (GAMs) are the predominant immune cells in the tumor microenvironment and drive immunosuppression. Strategies depleting GAMs have not demonstrated efficacy in clinical trials for GBM. It is critical …
View article: IMMU-42. PP2A-INHIBITION INDUCES STING-TYPE I-MEDIATED IMMUNOLOGIC CELL DEATH IN GBM
IMMU-42. PP2A-INHIBITION INDUCES STING-TYPE I-MEDIATED IMMUNOLOGIC CELL DEATH IN GBM Open
Glioblastoma (GBM) is one of the most lethal forms of brain cancer, and is known to be an aggressive, immunologically cold tumor, resulting in a lack of T-cell infiltration and killing. Thus increasing immune-mediated killing of GBM is a p…
View article: 1460 PP2Ac deficiency enhances tumor immunogenicity by activating STING-Type I interferon signaling in glioblastoma
1460 PP2Ac deficiency enhances tumor immunogenicity by activating STING-Type I interferon signaling in glioblastoma Open
Background Glioblastoma (GBM) is an immunologically 'cold' tumor that does not respond to current immunotherapy. Low immunogenicity of GBM with minimal MHC-I expression and paucity of T cells infiltration are major barriers for effective i…
View article: Supplementary Data from PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING–Type I Interferon Signaling in Glioblastoma
Supplementary Data from PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING–Type I Interferon Signaling in Glioblastoma Open
Cluster defining genes from scRNAseq data
View article: Supplementary Data from PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING–Type I Interferon Signaling in Glioblastoma
Supplementary Data from PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING–Type I Interferon Signaling in Glioblastoma Open
Supplementary Text Figs. S1 to S8 Tables S1 to S3
View article: Data from PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING–Type I Interferon Signaling in Glioblastoma
Data from PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING–Type I Interferon Signaling in Glioblastoma Open
Glioblastoma (GBM) is an immunologically “cold” tumor that does not respond to current immunotherapy. Here, we demonstrate a fundamental role for the α-isoform of the catalytic subunit of protein phosphatase-2A (PP2Ac) in regulating glioma…
View article: Supplementary Data from PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING–Type I Interferon Signaling in Glioblastoma
Supplementary Data from PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING–Type I Interferon Signaling in Glioblastoma Open
Cluster defining genes from scRNAseq data
View article: Supplementary Data from PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING–Type I Interferon Signaling in Glioblastoma
Supplementary Data from PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING–Type I Interferon Signaling in Glioblastoma Open
Supplementary Text Figs. S1 to S8 Tables S1 to S3
View article: Data from PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING–Type I Interferon Signaling in Glioblastoma
Data from PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING–Type I Interferon Signaling in Glioblastoma Open
Glioblastoma (GBM) is an immunologically “cold” tumor that does not respond to current immunotherapy. Here, we demonstrate a fundamental role for the α-isoform of the catalytic subunit of protein phosphatase-2A (PP2Ac) in regulating glioma…
View article: PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING–Type I Interferon Signaling in Glioblastoma
PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING–Type I Interferon Signaling in Glioblastoma Open
Glioblastoma (GBM) is an immunologically “cold” tumor that does not respond to current immunotherapy. Here, we demonstrate a fundamental role for the α-isoform of the catalytic subunit of protein phosphatase-2A (PP2Ac) in regulating glioma…
View article: PP2Ac/STRN4 negatively regulates STING-type I IFN signaling in tumor-associated macrophages
PP2Ac/STRN4 negatively regulates STING-type I IFN signaling in tumor-associated macrophages Open
Stimulator of IFN genes type I (STING-Type I) IFN signaling in myeloid cells plays a critical role in effective antitumor immune responses, but STING agonists as monotherapy have shown limited efficacy in clinical trials. The mechanisms th…