Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Bortezomib induces cell apoptosis and increases the efficacy of αPD-1 in BCR::ABL T315I mutation CML by targeting UBE2Q1.

International immunopharmacology - 25 Dec 2024

Jiang Fengyu, Liu Wenjie, Zhou Yanyu, Lin Siwei, Zhang Qin, Zhang Wan, Xue Yangyang, Li Cenming, Gao Anran, Shao Miaomiao, Liao Shanting, Ma Tonghui, Yu Xiaoxuan

Abstract excerpt

The BCR:ABL T315I mutation presents a significant challenge in the current management of Chronic Myeloid Leukemia (CML), highlighting the need to identify novel targets and drugs. In our study, we observed the elevated expression of UBE2Q1 in KBM5-T315I cells compared to KBM5 cells, where it interacted with DDX3, regulating its ubiquitination. Furthermore, we found that Bortezomib (BTZ) targeted UBE2Q1, reducing...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Bortezomib
Share to Drug Synergism

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Fusion Proteins, bcr-abl

Share to Leukemia, Myelogenous, Chronic, BCR-ABL Positive

Share to Mice, Inbred NOD

Share to Mice, SCID

Share to Programmed Cell Death 1 Receptor

Share to Ubiquitin-Conjugating Enzymes

Source

Identifiers

PMID: 39454411
DOI: 10.1016/j.intimp.2024.113311

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Bortezomib induces cell apoptosis and increases the efficacy of αPD-1 in BCR::ABL T315I mutation CML by targeting UBE2Q1.PMID 39454411Read ↗

The UBE2J2/UBE2K-MARCH5 ubiquitination machinery regulates apoptosis in response to venetoclax in acute myeloid leukemiaSemantic proximity Read ↗

HS-543 induces apoptosis of Imatinib-resistant chronic myelogenous leukemia with T315I mutation.Semantic proximity Read ↗

Discovery of Berberine that Targetedly Induces Autophagic Degradation of both BCR-ABL and BCR-ABL T315I through Recruiting LRSAM1 for Overcoming Imatinib ResistanceSemantic proximity Read ↗

MPT0B002, a novel microtubule inhibitor, downregulates T315I mutant Bcr-Abl and induces apoptosis of imatinib-resistant chronic myeloid leukemia cells.Semantic proximity Read ↗

Structure optimization, synthesis and bioactivity evaluation of novel BCR-ABL tyrosine kinase inhibitor targeting T315I mutation.Semantic proximity Read ↗

PBA2, a novel inhibitor of imatinib-resistant BCR-ABL T315I mutation in chronic myeloid leukemia.Semantic proximity Read ↗

Efficacy of a novel BCL-xL degrader, DT2216, in preclinical models of JAK2-mutated post-MPN AML.Semantic proximity Read ↗

Celastrol, a novel HSP90 inhibitor, depletes Bcr-Abl and induces apoptosis in imatinib-resistant chronic myelogenous leukemia cells harboring T315I mutation.Semantic proximity Read ↗

Combination of axitinib with dasatinib improves the outcome of a chronic myeloid leukemia patient with BCR-ABL1 T315I mutation.Semantic proximity Read ↗

26S Proteasome Non-ATPase Regulatory Subunits 1 (PSMD1) and 3 (PSMD3) as Putative Targets for Cancer Prognosis and TherapySemantic proximity Read ↗

The novel anticancer agent JNJ-26854165 is active in chronic myeloid leukemic cells with unmutated BCR/ABL and T315I mutant BCR/ABL through promoting proteosomal degradation of BCR/ABL proteins.Semantic proximity Read ↗

Proteasome 26S subunit, non-ATPases 1 (PSMD1) and 3 (PSMD3), play an oncogenic role in chronic myeloid leukemia by stabilizing nuclear factor-kappa BSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.