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  • PER2 interaction with HSP70 promotes cuproptosis in oral . . . - Nature
    Activating transcription factor 3 (ATF3) is an upstream regulator of PER2, that binds to the −807 to −796 bp site of the PER2 promoter Overexpression of ATF3 in vitro and in vivo is
  • PER2 integrates circadian disruption and pituitary tumorigenesis
    Our study suggests the core clock component PER2 as a novel common drug target for management of GHPA and PRLPA because PER2 acts as a pro-oncogenic protein for these two types of pituitary adenomas and the small molecule SR8278 decreases PER2 expression and mitigates tumor growth
  • The circadian clock gene PER2 plays an important role in tumor . . .
    PER2 knockdown increased the expression of Ki-67, MDM2, c-Myc, Bcl-2, MMP2, and VEGF mRNA (P<0 05), and decreased the expression of p53, Bax, and TIMP-2 mRNA (P<0 05) The in vivo experiments also proved that the tumorigenicity of SCC15 cells was significantly enhanced after PER2 silence (P<0 05)
  • Effects of Per2 overexpression on growth inhibition and metastasis, and . . .
    Per2 overexpression, via exogenous infusion reduced the ovarian cancer growth rate, which was demonstrated by a significant increase in the tumor inhibition rate In addition, Per2 may inhibit the expression of MTA-1 and promote the expression of nm23-H1 to restrict ovarian tumor growth and metastasis
  • PER2 expression and cellular localization play a critical role in tumor . . .
    PER2 expression levels were assessed by quantitative real-time reverse transcription polymerase chain reaction and immunofluorescence, together with markers of epithelial-mesenchymal transition, casein kinase 1ε (CK1ε), and tumor protein p53
  • Loss of the clock gene PER2 is associated with cancer development and . . .
    In the present study, we detected the mRNA and protein expression levels of PER2, PIK3CA, PTEN, P53, P14ARF and caspase‑8 in OSCC tissues and cancer-adjacent oral mucosa by reverse transcription-quantitative PCR (RT-qPCR), western blotting and immunohistochemistry
  • PER2 binding to HSP90 enhances immune response against oral squamous . . .
    Mechanistically, PER2 binds to heat shock protein 90 (HSP90) through the PAS1 domain and reduces the interaction of HSP90 with inhibitors of kappa B kinase (IKKs), promoting the ubiquitination of IKKα β and p65 nuclear translocation to inhibit IKK NF-κB pathway, thereby suppressing PD-L1 expression
  • Pro-inflammatory cytokines IL-6 and CCL2 suppress expression of . . .
    We found that acute stimulation by IL-6 CCL2 reduced PER2 expression in non-tumorigenic breast epithelial cells Longer term exposure to IL-6 CCL2 suppressed PER2 to an even lower level IL-6 activated STAT3 NFκB p50 signaling to recruit HDAC1 to the PER2 promoter
  • PER2 inhibits proliferation and stemness of glioma stem cells via the . . .
    Circadian clock gene, period circadian clock 2 (PER2) expression has been revealed to be inhibited in various types of cancer However, the precise role and potential mechanisms of PER2 in GSCs remains unclear
  • PER2 interaction with HSP70 promotes cuproptosis in oral . . . - PubMed
    These findings reveal a critical role of ATF3-dependent regulation of cuproptosis by PER2 in OSCC development, suggesting targeted upregulation of PER2 or ATF3 in combination to induce cuproptosis as a novel strategy to potentially improve the prognosis of OSCC patients
  • Clock genes and cancer - PubMed
    We propose that Period clock gene mutations promote tumorigenesis by unique molecular pathways Per2 and Per1 modulate beta-catenin and cell proliferation in colon and non-colon cancer cells Per2 mutation increases intestinal beta-catenin levels and colon polyp formation
  • PER2 binding to HSP90 enhances immune response against oral squamous . . .
    Mechanistically, PER2 binds to heat shock protein 90 (HSP90) through the PAS1 domain and reduces the interaction of HSP90 with inhibitors of kappa B kinase (IKKs), promoting the ubiquitination of IKKα β and p65 nuclear translocation to inhibit IKK NF-κB pathway, thereby suppressing PD-L1 expression
  • Cancer-associated fibroblasts promote drug resistance in
    In addition to tumor cell-intrinsic resistance mechanisms, accumulating evidence suggests that cancer-associated fibroblasts (CAFs) within the tumor microenvironment contribute to therapy resistance This study aimed to investigate CAF-driven molecular networks that shape the therapeutic susceptibility of ALK -driven lung adenocarcinoma cells
  • PER2 binding to HSP90 enhances immune response against oral squamous . . .
    Mechanistically, PER2 binds to heat shock protein 90 (HSP90) through the PAS1 domain and reduces the interaction of HSP90 with inhibitors of kappa B kinase (IKKs), promoting the ubiquitination of IKKα β and p65 nuclear translocation to inhibit IKK NF-κB pathway, thereby suppressing PD-L1 expression
  • A pyrimidine metabolism-related gene signature for prognosis prediction . . .
    Background Metabolic reprogramming is a hallmark in cancer Pyrimidine metabolism (PM), a part of nucleotide metabolism, has been shown to be associated with the progression of various cancers, and the prognostic predictive ability of pyrimidine metabolism-related genes (PMG) in breast cancer has not been elucidated This paper was designed to identify pyrimidine metabolism-related prognostic





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