Helicase-like transcription factor-deletion from the tumor microenvironment in a cell line-derived xenograft model of colorectal cancer reprogrammed the human transcriptome-S-nitroso-proteome to promote inflammation and redirect metastasis.
Helicase-Like Transcription Factor HLTF and E3 Ubiquitin Ligase SHPRH Confer DNA Damage Tolerance through Direct Interactions with Proliferating Cell Nuclear Antigen (PCNA).
HLTF E259K germline mutation induces accumulation of DNA double-strand breaks possibly through impaired PCNA polyubiquitination and is associated with myelodysplastic syndromes.
Study suggest that HLTF functions as a tumor suppressor gene in colorectal cancer (CRC). HLTF downregulation promotes the migration and invasion of CRC cells in vitro. Furthermore HLTF expression is negatively associated with overall survival in patients with CRC. HLTF may suppress the migration and invasion of CRC cells by targeting TGFbeta/SMAD signaling.
Data suggest that HIV-1 vpr mediates polyubiquitination of HLTF by directly loading it onto C-terminal WD40 domain of DCAF1 in complex the CRL4 an E3 ubiquitin ligase. (vpr = vpr gene product of Human immunodeficiency virus 1; HLTF = human helicase like transcription factor; DCAF1 = human Vpr (HIV-1) binding protein; CRL4 = human E3 ubiquitin ligase CRL4)
depletion of SMARCAL1 a SNF2-family DNA translocase that remodels stalled forks restores replication fork stability and reduces the formation of replication stress-induced DNA breaks and chromosomal aberrations in BRCA1/2-deficient cells. In addition to SMARCAL1 other SNF2-family fork remodelers including ZRANB3 and HLTF cause nascent DNA degradation and genomic instability
ALDH1A1 overexpression was found to enhance Lysosomal autophagy inhibitors (LAI) cell entry and cytotoxicity without directly affecting lysosome function or autophagic flux. Expression of HLTF allows repair of DNA damage caused by LAI-induced reactive oxygen species leading to hydroxychloroquine resistance.
A large number of SNF2 family DNA and ATP-dependent motor proteins are needed during transcription DNA replication and DNA repair to manipulate protein-DNA interactions and change DNA structure. SMARCAL1 ZRANB3 and HLTF are three related members of this family with specialized functions that maintain genome stability during DNA replication. (review)
the present study does not provide any strong evidence that PAI-1 gene variants are implicated in the risk of DR or the development of DR during T2DM course.
Fasudil reduced LPS-mediated TF and PAI-1 expression and activity in PBMCs. These effects may partially be relevant to the clinical benefits of fasudil in the treatment of CAPD patients.
HIV-1 vpr reprograms CRL4(DCAF1) E3 to direct HLTF for proteasome-dependent degradation independent from previously reported Vpr interactions with base excision repair enzyme uracil DNA glycosylase (UNG2) and crossover junction endonuclease MUS81 which Vpr also directs for degradation via CRL4(DCAF1) E3.
HLTF is degraded in lymphocytic cells and macrophages infected with Vpr-expressing HIV-1. Our results reveal a previously unidentified strategy for HIV-1 to antagonize DNA repair in host cells.
HLTF expression is altered in various cancers via two mechanisms: gene silencing through promoter hypermethylation or alternative mRNA splicing which leads to the expression of truncated proteins that lack DNA repair domains. (review)
HLTF promotes the filling-in of gaps left opposite damaged DNA during replication and this postreplication repair function depends on its HIRAN domain.
These results suggest that the HIRAN domain functions as a sensor to the 3'-end of the primer strand at the stalled replication fork and that the domain facilitates fork regression.
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