Xu Luo

ORCID: 0009-0002-3351-6305
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About
Contact & Profiles
Research Areas
  • Cell death mechanisms and regulation
  • Mitochondrial Function and Pathology
  • MicroRNA in disease regulation
  • RNA Interference and Gene Delivery
  • Autophagy in Disease and Therapy
  • Cancer-related Molecular Pathways
  • Ubiquitin and proteasome pathways
  • ATP Synthase and ATPases Research
  • DNA Repair Mechanisms
  • Genomics and Chromatin Dynamics
  • NF-κB Signaling Pathways
  • RNA modifications and cancer
  • Inflammasome and immune disorders
  • Wound Healing and Treatments
  • Corneal Surgery and Treatments
  • interferon and immune responses
  • Ferroptosis and cancer prognosis
  • Acute Kidney Injury Research
  • Mesenchymal stem cell research
  • Metabolism and Genetic Disorders
  • Epigenetics and DNA Methylation
  • Cancer, Lipids, and Metabolism
  • Circular RNAs in diseases
  • Trace Elements in Health
  • Intracerebral and Subarachnoid Hemorrhage Research

University of Nebraska Medical Center
2010-2024

Xuzhou Medical College
2024

Dalian Medical University
2020-2024

First Affiliated Hospital of Dalian Medical University
2024

Wenzhou Medical University
2012-2023

First Affiliated Hospital of Wenzhou Medical University
2012-2023

Chongqing Medical University
2020-2023

Second Affiliated Hospital of Chongqing Medical University
2020-2023

Zhejiang Hospital
2023

City University of Hong Kong
2022

We report here the reconstitution of a pathway that leads to apoptotic changes in nuclei by using recombinant DNA fragmentation factor (DFF), heterodimeric protein 40 and 45 kDa. Coexpression DFF40 DFF45 is required generate DFF, which becomes activated when cleaved caspase-3. The fragments dissociate from DFF40, active component DFF. Purified exhibited an intrinsic DNase activity was markedly stimulated chromatin-associated proteins histone H1 high mobility group proteins. also triggered...

10.1073/pnas.95.15.8461 article EN Proceedings of the National Academy of Sciences 1998-07-21

During apoptosis, the BCL-2-family protein tBID promotes mitochondrial permeabilization by activating BAX and BAK blocking anti-apoptotic BCL-2 members. Here, we report that can also mediate itself, resulting in release of cytochrome c DNA, caspase activation apoptosis even absence BAK. This previously unrecognized activity depends on helix 6, homologous to pore-forming regions BAK, be blocked pro-survival proteins. Importantly, tBID-mediated independent is physiologically relevant for SMAC...

10.15252/embj.2021108690 article EN cc-by The EMBO Journal 2021-12-21

Hypertrophic scars (HTS) and keloids are challenging problems. Their pathogenesis results from an overproduction of fibroblasts excessive deposition collagen. Studies suggest a possible anti-scarring effect basic fibroblast growth factor (bFGF) during wound healing, but the precise mechanisms bFGF still unclear. In view this, we investigated therapeutic effects on HTS animal model as well human scar (HSF) model. We show that promoted healing reduced area flattened non-pathological in rat...

10.1371/journal.pone.0059966 article EN cc-by PLoS ONE 2013-04-02

Abstract BH3-mimetics are a new class of anti-cancer drugs that inhibit anti-apoptotic Bcl-2 proteins. In doing so, sensitise to cell death. Venetoclax is potent, BCL-2 selective BH3-mimetic clinically approved for use in chronic lymphocytic leukaemia. has also been shown mitochondrial metabolism, this consistent with proposed role metabolic regulation. We used venetoclax understand function. Similar others, we found inhibited respiration. addition, impairs TCA cycle activity leading...

10.1038/s41419-020-02867-2 article EN cc-by Cell Death and Disease 2020-08-13

USF1 and USF2 are basic helix-loop-helix transcription factors implicated in the control of cellular proliferation. In HeLa cells, USF proteins transcriptionally active their overexpression causes marked growth inhibition. contrast, had essentially no effect on proliferation Saos-2 osteosarcoma cell line. also lacked transcriptional activity cells when assayed by transient cotransfection with USF-dependent reporter genes. Yet, there was difference expression, subcellular localization, or...

10.1128/mcb.19.2.1508 article EN Molecular and Cellular Biology 1999-02-01

USF is a family of basic helix-loop transcriptional factors that recognizes DNA-binding sites similar to those the Myc oncoproteins. Here, various functional domains in mouse USF2 protein were identified and characterized. Indirect immunofluorescence studies with transiently transfected cells revealed both region highly conserved USF-specific (USR) are involved nuclear localization USF2. Cotransfection assays deletion mutants containing domain either or GAL4 two distinct activation USF2, USR...

10.1128/mcb.16.4.1367 article EN Molecular and Cellular Biology 1996-04-01

Homo-oligomerization of Bax (or Bak) has been hypothesized to be responsible for cell death through the mitochondria-dependent apoptosis pathway. However, partly due a lack structural information on homo-oligomerization and inducing domain(s), this hypothesis remained difficult test. In study, we identified three-helix unit, comprised BH3 (helix 2) BH1 domains 4 helix 5), as domain Bax. When targeted mitochondria, minimum oligomerization unit induced in −/− Bak mouse embryonic fibroblasts...

10.1101/gad.1553607 article EN Genes & Development 2007-08-01

<ns4:p>Bax and Bak, two functionally similar, pro-apoptotic proteins of the Bcl-2 family, are known as gateway to apoptosis because their requisite roles effectors mitochondrial outer membrane permeabilization (MOMP), a major step during mitochondria-dependent apoptosis. The mechanism how cells turn Bax/Bak from inert molecules into fully active lethal had long been focal point debate centered around competing, but not mutually exclusive, models: direct activation indirect activation. After...

10.12688/f1000research.25607.1 preprint EN cc-by F1000Research 2020-08-06

The impressive selectivity and efficacy of BH3 mimetics for treating cancer has largely been limited to BCL-2 dependent hematological malignancies. Most solid tumors depend on other anti-apoptotic proteins, including MCL-1, survival. recent description S63845 as the first specific potent MCL-1 inhibitor represents an important therapeutic advance, since is not targeted by currently available mimetics, Navitoclax or Venetoclax, commonly associated with chemoresistance. In this study, we...

10.1038/s41418-018-0183-7 article EN cc-by Cell Death and Differentiation 2018-09-05

USF is a family of transcription factors characterized by highly conserved basic-helix-loop-helix-leucine zipper (bHLH-zip) DNA-binding domain. Two different genes, termed USF1 and USF2, are ubiquitously expressed in both humans mice. The USF2 proteins contain divergent transcriptional activation domains but share extensive homologies the bHLH-zip region recognize same CACGTG DNA motifs. Although activities these have been characterized, biological function not well understood. Here, focus-...

10.1073/pnas.93.3.1308 article EN Proceedings of the National Academy of Sciences 1996-02-06

The mechanisms governing the function of cellular USF and herpesvirus immediate-early transcription factors are subjects considerable interest. In this regard, we identified a novel form coordinate gene regulation involving cooperative interplay between varicella-zoster virus protein 62 (IE 62). A single USF-binding site defines potential level IE 62-dependent activation bidirectional viral early promoter DNA polymerase major DNA-binding genes. We also report dominant negative USF-2 mutant...

10.1128/mcb.14.10.6896 article EN Molecular and Cellular Biology 1994-10-01

Abstract Cells experiencing delays in mitotic progression are prone to undergo apoptosis unless they can exit mitosis before proapoptotic factors reach a critical threshold. Microtubule targeting agents (MTAs) arrest cells and induce apoptotic cell death engaging the BCL2 network. Degradation of antiapoptotic family member MCL-1 is considered set time until onset upon MTA treatment. MCL1 degradation involves its interaction with one key binding partners, BH3-only protein NOXA. Here, we...

10.1038/s41418-020-0503-6 article EN cc-by Cell Death and Differentiation 2020-02-03

Abstract In this study, microarray data analysis, real‐time quantitative PCR and immunohistochemistry were used to detect the expression levels of SSRP1 in colorectal cancer (CRC) tissue corresponding normal tissue. The association between structure‐specific recognition protein 1 (SSRP1) patient prognosis was examined by Kaplan‐Meier analysis. knocked down overexpressed CRC cell lines, its effects on proliferation, cycling, migration, invasion, cellular energy metabolism, apoptosis,...

10.1111/jcmm.14134 article EN cc-by Journal of Cellular and Molecular Medicine 2019-02-14

Ferroptosis has been implicated in the pathogenesis of secondary brain injury following intracerebral hemorrhage (ICH), and regulating this process is considered a potential therapy for alleviating further injury. A previous study showed that CDGSH iron sulfur domain 2 (CISD2) can inhibit ferroptosis cancer. Thus, we investigated effects CISD2 on mechanisms underlying its neuroprotective role mice after ICH. expression markedly increased over-expression significantly decreased number...

10.1111/jnc.15785 article EN Journal of Neurochemistry 2023-02-18

Master regulators, such as Sox2, Oct4 and Nanog, control complex gene networks necessary for the self-renewal pluripotency of embryonic stem cells (ESC). These master regulators associate with co-activators co-repressors to precisely their targets. Recent studies using proteomic analysis have identified a large, diverse group that including Sox2. In this report, we examined size distribution nuclear protein complexes containing Sox2 its associated proteins HDAC1, Sall4 Lin28. Interestingly,...

10.1371/journal.pone.0015486 article EN cc-by PLoS ONE 2010-11-12

How most apoptotic stimuli trigger mitochondrial dysfunction remains to be resolved. We screened the entire Bcl-2 network for its involvement in DNA damage-induced apoptosis HeLa cells. Although anti-apoptotic member Bcl-xL served as a major suppressor, initiated only when both Mcl-1 and were eliminated. The pro-apoptotic members Bak, Bad, Bim, Noxa required induced by damaging agents camptothecin UV. We, therefore, used His-tagged expression system capture relevant BH3-only proteins that...

10.1074/jbc.m109.086231 article EN cc-by Journal of Biological Chemistry 2010-03-12
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