ORCID Profile
0000-0003-0960-6546
Current Organisation
Dana Farber Cancer Institute
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Publisher: American Association for Cancer Research (AACR)
Date: 04-2019
DOI: 10.1158/0008-5472.CAN-18-2965
Abstract: Since the identification of the first RNA demethylase and the establishment of methylated RNA immunoprecipitation-sequencing methodology 6 to 7 years ago, RNA methylation has emerged as a widespread phenomenon and a critical regulator of transcript expression. This new layer of regulation is termed “epitranscriptomics.” The most prevalent RNA methylation, N6-methyladenosine (m6A), occurs in approximately 25% of transcripts at the genome-wide level and is enriched around stop codons, in 5′- and 3′-untranslated regions, and within long internal exons. RNA m6A modification regulates RNA splicing, translocation, stability, and translation into protein. m6A is catalyzed by the RNA methyltransferases METTL3, METTL14, and METTL16 (writers), is removed by the demethylases FTO and ALKBH5 (erasers), and interacts with m6A-binding proteins, such as YTHDF1 and IGF2BP1 (readers). RNA methyltransferases, demethylases, and m6A-binding proteins are frequently upregulated in human cancer tissues from a variety of organ origins, increasing onco-transcript and oncoprotein expression, cancer cell proliferation, survival, tumor initiation, progression, and metastasis. Although RNA methyltransferase inhibitors are not available yet, FTO inhibitors have shown promising anticancer effects in vitro and in animal models of cancer. Further screening for selective and potent RNA methyltransferase, demethylase, or m6A-binding protein inhibitors may lead to compounds suitable for future clinical trials in cancer patients.
Publisher: Wiley
Date: 23-12-2023
Abstract: Photoluminescence quantum yield ( ϕ ) is a key parameter of any luminescent material. There are two main ways to determine this value: 1) absolute, which requires calculation of the number of emitted and absorbed photons and 2) relative, which utilizes the emission of a reference s le with known ϕ . Both methods become more complicated in case of upconversion (UC) photoluminescence, due to its nonlinear nature. The main obstacle to employing the relative method is the lack of a suitable reference with known UC quantum yield (UCQY, ϕ UC ). Herein, a new UCQY reference material is presented, based on SrF 2 :1%Yb 3+ ,1%Er 3+ single crystal, for the relative measurement of ϕ UC for near‐infrared (976 nm)‐to‐visible UC. When utilizing this reference material, the ϕ UC is determined to be 2.5% (at 100 W cm −2 ) for α‐NaYF 4 :18%Yb 3+ ,2%Er 3+ @CaF 2 nanocrystals (NCs). This result coincides very well with the value for the same NCs determined using the absolute method of ϕ UC = 2.4% (at 100 W cm −2 ). The intensity dependence of UCQY yield for the NCs determined using the SrF 2 :1%Yb 3+ ,1%Er 3+ reference exhibits good agreement with the results acquired with the absolute method. In addition, various effects that can have an impact on the measured UCQY using absolute and relative methods are discussed.
Publisher: Oxford University Press (OUP)
Date: 06-08-2020
DOI: 10.1093/NAR/GKAA653
Abstract: The IGF2 mRNA-binding protein 1 (IGF2BP1) is a non-catalytic post-transcriptional enhancer of tumor growth upregulated and associated with adverse prognosis in solid cancers. However, conserved effector pathway(s) and the feasibility of targeting IGF2BP1 in cancer remained elusive. We reveal that IGF2BP1 is a post-transcriptional enhancer of the E2F-driven hallmark in solid cancers. IGF2BP1 promotes G1/S cell cycle transition by stabilizing mRNAs encoding positive regulators of this checkpoint like E2F1. This IGF2BP1-driven shortening of the G1 cell cycle phase relies on 3′UTR-, miRNA- and m6A-dependent regulation and suggests enhancement of cell cycle progression by m6A-modifications across cancers. In addition to E2F transcription factors, IGF2BP1 also stabilizes E2F-driven transcripts directly indicating post-transcriptional ‘super’-enhancer role of the protein in E2F-driven gene expression in cancer. The small molecule BTYNB disrupts this enhancer function by impairing IGF2BP1-RNA association. Consistently, BTYNB interferes with E2F-driven gene expression and tumor growth in experimental mouse tumor models.
Publisher: Elsevier BV
Date: 2021
No related grants have been discovered for Jacob Haase.