Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P05412 (c-Jun)
 11,453 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

F-box and WD repeat domain-containing protein 7 (FBW7), also known as FBXW7, AGO or hCDC4, is an F-box protein with seven tandem WD40 repeats. FBW7 is a key substrate recognition subunit of the Skp1-Cul1-F-box-protein E3 ubiquitin ligase. FBW7 targets for ubiquitination and destruction of numerous crucial transcription factors and protooncogenes, including cyclin E, c-Myc, c-Jun, Notch and MCL-1. FBW7 is a well-characterized tumor suppressor, and its gene is frequently mutated or deleted in various types of human cancer, including colorectal cancer, gastric cancer, ovarian cancer and different types of leukemia. Accumulating evidence indicates that the aberrant expression of FBW7 is involved in the development of hematological tumors, including T cell acute lymphoblastic leukemia, adult T cell leukemia/lymphoma, chronic lymphocytic leukemia and multiple myeloma. The present review will describe the latest findings on the role of FBW7 in hematological tumors, in order to identify a novel target for future therapies.
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PMID:FBW7 in hematological tumors. 3219 57

Ultraviolet A (UVA) is a major factor in skin aging and damage. Antioxidative materials may ameliorate this UV damage. This study investigated the protective properties of N-(4-bromophenethyl) caffeamide (K36H) against UVA-induced skin inflammation, apoptosis and genotoxicity in keratinocytes. The protein expression or biofactor concentration related to UVA-induced skin damage were identified using an enzyme-linked immunosorbent assay and western blotting. K36H reduced UVA-induced intracellular reactive oxygen species generation and increased nuclear factor erythroid 2-related factor 2 translocation into the nucleus to upregulate the expression of heme oxygenase-1, an intrinsic antioxidant enzyme. K36H inhibited UVA-induced activation of extracellular-signal-regulated kinases and c-Jun N-terminal kinases, reduced the overexpression of matrix metalloproteinase (MMP)-1 and MMP-2 and elevated the expression of the metalloproteinase-1 tissue inhibitor. Moreover, K36H inhibited the phosphorylation of c-Jun and downregulated c-Fos expression. K36H attenuated UVA-induced Bax and caspase-3 expression and upregulated antiapoptotic protein B-cell lymphoma 2 expression. K36H reduced UVA-induced DNA damage. K36H also downregulated inducible nitric oxide synthase, cyclooxygenase-2 and interleukin-6 expression as well as the subsequent generation of prostaglandin E2 and nitric oxide. We observed that K36H ameliorated UVA-induced oxidative stress, inflammation, apoptosis and antiphotocarcinogenic activity. K36H can potentially be used for the development of antiphotodamage and antiphotocarcinogenic products.
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PMID:Protection against Ultraviolet A-Induced Skin Apoptosis and Carcinogenesis through the Oxidative Stress Reduction Effects of N-(4-bromophenethyl) Caffeamide, A Propolis Derivative. 3232 32


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