Lin-Zhi Qi

ORCID: 0000-0002-5200-5466
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About
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Research Areas
  • Ubiquitin and proteasome pathways
  • NF-κB Signaling Pathways
  • Cancer-related Molecular Pathways
  • Protein Kinase Regulation and GTPase Signaling
  • DNA Repair Mechanisms
  • Cancer, Hypoxia, and Metabolism
  • Cancer Immunotherapy and Biomarkers
  • Bladder and Urothelial Cancer Treatments
  • Cancer-related gene regulation
  • Immune Response and Inflammation
  • Natural product bioactivities and synthesis
  • Epigenetics and DNA Methylation
  • Pancreatic and Hepatic Oncology Research
  • interferon and immune responses
  • Cell death mechanisms and regulation
  • Wnt/β-catenin signaling in development and cancer
  • Hepatitis B Virus Studies

Chongqing University
2022-2024

Wuhan University
2023

Abstract MAPK/JNK signaling is pivotal in carcinogenesis. However, ubiquitin-mediated homeostasis of JNK remains to be verified. Here, with results from RNA sequencing (RNA-seq) and luciferase reporter pathway identification, we show that USP14 orchestrates identify as a deubiquitinase interacts stabilizes JNK. elevated colorectal cancer patients positively associated protein downstream gene expression. ablation reduces cell proliferation vitro tumorigenesis vivo by downregulating...

10.1038/s41419-023-05579-5 article EN cc-by Cell Death and Disease 2023-01-24

Activation of the NF-κB pathway is strictly regulated to prevent excessive inflammatory and immune responses. In a well-known negative feedback model, IκBα-dependent termination delayed response pattern in later stage activation, mechanisms mediating rapid active remain unclear. Here, we showed IκBα-independent nuclear mediated by CLK2, which negatively phosphorylating RelA/p65 subunit at Ser180 nucleus limit its transcriptional activation through degradation export. Depletion CLK2 increased...

10.1038/s41467-024-48288-z article EN cc-by Nature Communications 2024-05-09

The catenin beta 1 gene (CTNNB1) plays a crucial role in the malignant progression of various cancers. Recent studies have suggested that CTNNB1 hyperactivation is closely related to occurrence and development bladder cancer (BCa). As member deubiquitinating enzyme (DUB) family, ubiquitin C-terminal hydrolase L3 (UCHL3) abnormally expressed In this study, we discovered UCHL3 novel oncogene cancer, suggesting it promising target against cancer.We utilized CRISPR‒Cas9 technology construct cell...

10.1186/s12967-023-04311-3 article EN cc-by Journal of Translational Medicine 2023-09-22

Abstract MAPK/JNK signaling is pivotal in carcinogenesis. However, ubiquitin-mediated homeostasis of JNK remains to be verified. Here, with results from RNA sequencing (RNA-seq) and luciferase reporter pathway identification, we show that USP14 orchestrates identify as a deubiquitinase interacts stabilizes JNK. elevated colorectal cancer patients positively associated protein downstream gene expression. ablation clearly inhibits tumorigenesis by targeting the cascade vitro vivo . Moreover,...

10.21203/rs.3.rs-1702021/v1 preprint EN cc-by Research Square (Research Square) 2022-07-01

<title>Abstract</title> The NF-κB transcription factor families play significant roles in both the inflammatory and immune responses. activation of pathway is subject to strict regulation prevent excessive While a widely accepted negative feedback model, IκBs-dependent termination observed as lagged response pattern later stage activation, prompt mechanisms active remain not fully clarified. Here, we show an IκBs-independent model nuclear that CLK2 negatively regulates by phosphorylating p65...

10.21203/rs.3.rs-3184196/v1 preprint EN cc-by Research Square (Research Square) 2023-08-18

Abstract Studies have suggested a close association between hyperactivation of the catenin beta 1 gene (CTNNB1) and occurrence progression colorectal cancer (CRC). Here, we report that Pyridoxal kinase (PDXK) promotes development through Wnt signaling pathway. The expression PDXK is elevated in CRC patients associated with an unfavourable prognosis. Genetic depletion significantly inhibited cell viability, migration both vitro vivo . Furthermore, observed overexpression enhanced invasion,...

10.21203/rs.3.rs-3505983/v1 preprint EN cc-by Research Square (Research Square) 2023-11-01
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