og:image: https://cdn.ncbi.nlm.nih.gov/pubmed/persistent/pubmed-meta-image.png twitter:card: summary og:site_name: PubMed keywords: pmid:36622366, doi:10.1042/BSR20222102, Research Support, Non-U.S. Gov't, Vasudha Tandon, Rita Moreno, Sourav Banerjee, Gene Expression Regulation, Humans, Neoplasms*, Phosphorylation, Proteasome Inhibitors / pharmacology, Transcription Factors / genetics, Transcription Factors / metabolism, PubMed Abstract, NIH, NLM, NCBI, National Institutes of Health, National Center for Biotechnology Information, National Library of Medicine, MEDLINE twitter:url: https://pubmed.ncbi.nlm.nih.gov/36622366/ citation_journal_title: Bioscience reports ncbi_pdid: abstract ncbi_phid: 579300011145644500002FF4104494B6.1.m_5 og:description: Preserving proteostasis is a major survival mechanism for cancer. Dual specificity tyrosine phosphorylation-regulated kinase 2 (DYRK2) is a key oncogenic kinase that directly activates the transcription factor heat-shock factor 1 (HSF1) and the 26S proteasome. Targeting DYRK2 has proven to be a trac ? og:image:secure_url: https://cdn.ncbi.nlm.nih.gov/pubmed/persistent/pubmed-meta-image.png ncbi_db: pubmed citation_issn: 1573-4935 ncbi_pinger_stat_url: https://www.ncbi.nlm.nih.gov/stat dc:title: Dual inhibition of HSF1 and DYRK2 impedes cancer progression - PubMed log_category: literature Content-Encoding: UTF-8 robots: index,nofollow,noarchive twitter:domain: pubmed.ncbi.nlm.nih.gov log_icons_present: true log_op: retrieve citation_abstract_html_url: https://pubmed.ncbi.nlm.nih.gov/36622366/ citation_issue: 1 log_source_db: pubmed log_displayeduids: 36622366 ncbi_uid: 36622366 citation_doi: 10.1042/BSR20222102 citation_volume: 43 Content-Language: en theme-color: #20558a citation_title: Dual inhibition of HSF1 and DYRK2 impedes cancer progression ncbi_sg_optimize_id: citation_publisher: Biosci Rep HandheldFriendly: True description: Preserving proteostasis is a major survival mechanism for cancer. Dual specificity tyrosine phosphorylation-regulated kinase 2 (DYRK2) is a key oncogenic kinase that directly activates the transcription factor heat-shock factor 1 (HSF1) and the 26S proteasome. Targeting DYRK2 has proven to be a trac ? citation_date: 01/31/2023 title: Dual inhibition of HSF1 and DYRK2 impedes cancer progression - PubMed ncbi_cost_center: pubmed twitter:image: https://cdn.ncbi.nlm.nih.gov/pubmed/persistent/pubmed-meta-image.png uid: 36622366 ncbi_pinger_gtm_track: true Content-Type: text/html; charset=UTF-8 X-Parsed-By: org.apache.tika.parser.DefaultParser og:type: website twitter:title: Dual inhibition of HSF1 and DYRK2 impedes cancer progression - PubMed citation_pmid: 36622366 ncbi_app: pubmed og:title: Dual inhibition of HSF1 and DYRK2 impedes cancer progression - PubMed citation_authors: Tandon V;Moreno R;Allmeroth K;Quinn J;Wiley SE;Nicely LG;Denzel MS;Edwards J;de la Vega L;Banerjee S; X-UA-Compatible: IE=edge referrer: origin-when-cross-origin MobileOptimized: 320 viewport: width=device-width, initial-scale=1.0 twitter:description: Preserving proteostasis is a major survival mechanism for cancer. Dual specificity tyrosine phosphorylation-regulated kinase 2 (DYRK2) is a key oncogenic kinase that directly activates the transcription factor heat-shock factor 1 (HSF1) and the 26S proteasome. Targeting DYRK2 has proven to be a trac ? og:url: https://pubmed.ncbi.nlm.nih.gov/36622366/