Results 71 to 80 of about 55,031 (288)

HNRNPK maintains epidermal progenitor function through transcription of proliferation genes and degrading differentiation promoting mRNAs. [PDF]

open access: yes, 2019
Maintenance of high-turnover tissues such as the epidermis requires a balance between stem cell proliferation and differentiation. The molecular mechanisms governing this process are an area of investigation.
Chen, Yifang   +8 more
core   +1 more source

A Patient‐Derived Organoid Biobank of Adamantinomatous Craniopharyngioma as a Platform for Drug Discovery

open access: yesAdvanced Science, EarlyView.
This study successfully establishes adamantinomatous craniopharyngioma (ACP) patient‐derived organoids (PDOs) that preserve the histopathological and genetic features of the original tumors. Through drug sensitivity assays and subsequent mechanistic analyses, the study demonstrates that Ceritinib exerts its inhibitory effects on ACP PDO growth by ...
Huarong Zhang   +15 more
wiley   +1 more source

Aging-associated changes in microRNA expression profile of internal anal sphincter smooth muscle: Role of microRNA-133a. [PDF]

open access: yes, 2016
A comprehensive genomic and proteomic, computational, and physiological approach was employed to examine the (previously unexplored) role of microRNAs (miRNAs) as regulators of internal anal sphincter (IAS) smooth muscle contractile phenotype and basal ...
Addya, Sankar   +6 more
core   +3 more sources

TRIM56 Aggravates Cerebral Ischemia‐Reperfusion Injury via Inhibiting KLF4‐Activated Ferroptosis Signaling

open access: yesAdvanced Science, EarlyView.
This study reveals that the E3 ubiquitin ligase TRIM56 exacerbates neuronal ferroptosis and brain damage by mediating K48‐linked ubiquitination and degradation of KLF4, leading to suppression of the xCT/GSH/GPX4 axis. Targeting TRIM56 alleviates cerebral ischemia‐reperfusion injury in vivo and in vitro, highlighting its therapeutic potential.
Qiangping Wang   +15 more
wiley   +1 more source

KLF4, a miR-32-5p targeted gene, promotes cisplatin-induced apoptosis by upregulating BIK expression in prostate cancer

open access: yesCell Communication and Signaling, 2018
Background Chemotherapeutic insensitivity remains a big challenge in prostate cancer treatment. Recently, increasing evidence has indicated that KLF4 plays a key role in prostate cancer.
Lu Zhang   +8 more
doaj   +1 more source

Prognostic significance of KLF4 expression in gastric cancer

open access: yesOncology Letters, 2016
To understand the roles of pluripotent stem cell-inducing genes in gastric cancer, the expression of Krüppel-like factor 4 (KLF4), Nanog, octamer-binding transcription factor 4 (Oct4), avian myelocytomatosis viral oncogene homolog (c-Myc) and sex-determining region Y-box 2 (SOX2) was examined using the newly developed gastric carcinoma tissue ...
Isaya, Hashimoto   +11 more
openaire   +3 more sources

Distinctive Klf4 mutants determine preference for DNA methylation status [PDF]

open access: yesNucleic Acids Research, 2016
Reprogramming of mammalian genome methylation is critically important but poorly understood. Klf4, a transcription factor directing reprogramming, contains a DNA binding domain with three consecutive C2H2 zinc fingers. Klf4 recognizes CpG or TpG within a specific sequence.
Hashimoto, Hideharu   +6 more
openaire   +2 more sources

ZNF750 is a lineage-specific tumour suppressor in squamous cell carcinoma. [PDF]

open access: yes, 2016
ZNF750 controls epithelial homeostasis by regulating epidermal-differentiation genes, a role underscored by its pathogenic mutations in esophageal squamous cell cancers (SCCs). However, the precise role of ZNF750 in SCC cell biology remains unclear.
Chen, Y   +15 more
core   +2 more sources

Human Atlas of Tooth Decay Progression: Identification of Cellular Mechanisms Driving the Switch from Dental Pulp Repair Toward Irreversible Pulpitis

open access: yesAdvanced Science, EarlyView.
Tooth decay progression transforms the dental pulp response from repair to fibrosis. At early stages, stromal cells reprogram to repair the extra cellular matrix (ECM), blood vessels, and nerves, remodel and grow, keeping repair possible. In advanced decay, hypoxia, and vessel regression, in complement with an immune switch, fuel nerve degeneration and
Hoang Thai Ha   +12 more
wiley   +1 more source

Promoter hypermethylation of KLF4 inactivates its tumor suppressor function in cervical carcinogenesis. [PDF]

open access: yesPLoS ONE, 2014
OBJECTIVE: The KLF4 gene has been shown to be inactivated in cervical carcinogenesis as a tumor suppressor. However, the mechanism of KLF4 silencing in cervical carcinomas has not yet been identified.
Wen-Ting Yang, Peng-Sheng Zheng
doaj   +1 more source

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