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Wolf Lab for Tumor Biochemistry @_WolfLab

#MYC_Cancer #systemsbiology at @Uni_WUE with @NevenkaDudvars1 @MV4_11 @_BikashAdhikari @J_Hofstetter1 @ashwin_narain @PranjScripts @EingLorenz

Joined March 2019
  • Tweets 299
  • Following 125
  • Followers 437
41 Photos and videos
We are recruiting: ERC- and DFG-funded PhD positions in Tumor Biology (Kiel, Germany). We look forward to your application!
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Our latest paper describing a role for SCAF1 in promoting RNAPII elongation is online at Nucleic Acids Research @NAR_Open! Check it out here: doi.org/10.1093/nar/gkae1219. Big thanks to collaborators @erhard_lab, @MYCGyvers and AG Schlosser!

Phenotypic screens identify SCAF1 as critical activator of RNAPII elongation and global transcrip...

Abstract. Transcripts produced by RNA polymerase II (RNAPII) are fundamental for cellular responses to environmental changes. It is therefore no surprise t

academic.oup.com
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Our new manuscript has been published in eLife. We describe a new method for identifying suitable E3 ligases for PROTACs. Many thanks to everyone involved. pubmed.ncbi.nlm.nih.gov/3964…

Identification of suitable target/E3 ligase pairs for PROTAC development using a rapamycin-induced...

The development of proteolysis targeting chimeras (PROTACs), which induce the degradation of target proteins by bringing them into proximity with cellular E3 ubiquitin ligases, has revolutionized...

pubmed.ncbi.nlm.nih.gov
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Wolf Lab for Tumor Biochemistry retweeted
vosslab@voss_lab
26 Nov 2024
Out now: Our collaborative #Golgi #glycotime story, which shows (i) that B4GALT5, a Golgi enzyme, is subject to M6P tagging and (ii) that GOLPH3/GOLPH3L stabilize LYSET and the GlcNAc-phosphotranferase complex and thus are crucial to cellular M6P tagging. tinyurl.com/jkv26nhh
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Our new paper on TTK/Aurora PROTACs is out: pubmed.ncbi.nlm.nih.gov/3953… Great collaboration with the Sarli lab. Thanks to all involved!"

Development of 2-Aminoadenine-Based Proteolysis-Targeting Chimeras (PROTACs) as Novel Potent...

Monopolar spindle 1 (Mps1, also known as TTK) and Aurora kinase (AURK) A and B are critical regulators of mitosis and have been linked to the progression of various cancers. Here, we report the...

pubmed.ncbi.nlm.nih.gov
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Congratulations @_MarkusVogt for delivering a superb PhD defense!!!🍾🥂
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Wolf Lab for Tumor Biochemistry retweeted
Lucas Farnung@LucasFarnung
1 Nov 2024
I have written a concise review on chromatin transcription as part of the @JMolBiol special issue on transcription elongation. Check it out! authors.elsevier.com/sd/arti…
Mechanisms of nucleosome retention and/or transfer during transcription elongation.

ALT Mechanisms of nucleosome retention and/or transfer during transcription elongation.
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We congratulate Michaela Reissland and the whole team in Markus Diefenbacher's lab on their new paper in Oncogene. In the study, they were able to demonstrate the role of USP10 in Wnt signalling in colorectal cancer models. Thank you for the opportunity to contribute.
Oncogene Journal@oncogenejournal
27 Oct 2024
USP10 emerges as a unique therapeutic target in APC-truncated #ColorectalCancer 🔬nature.com/articles/s41388-0… @DiefenbacherL #OpenAccess
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Congratulations, Lorenz!
Eilers Lab@MYCGyvers
20 Sep 2024
PhDone ✅ @EingLorenz finally defended his defense. After his PhD in the @_WolfLab he is now working as a Postdoc in our Lab! Fantastic defense and as always a good party afterwards!
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Wolf Lab for Tumor Biochemistry retweeted
Gut Journal
@Gut_BMJ
13 Aug 2024
#GUTAbstract by @_MarkusVogt @_WolfLab et al on "Targeting MYC effector functions in pancreatic cancer by inhibiting the ATPase RUVBL1/2" via bit.ly/3SNQbX0 Paper: bit.ly/3M5SqkW @DiefenbacherL @NevenkaDudvars1 #Pancreas #PancreaticCancer
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Graduate students and postdocs interested in PROTACs and Glues: Register for the AEK workshop November 4-6 in Berlin with outstanding international speakers: aek-conferences.org/autumnsc…
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Many thanks to the press office of Kiel University for the press release about our new paper in GUT: uni-kiel.de/de/detailansicht…
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Wolf Lab for Tumor Biochemistry retweeted
Rapé Lab@RapeLab
16 Jun 2024
Congratulations to the amazing team at @Nurix_Tx for the continued success of their brain-penetrant BTK degrader in the clinic! ir.nurixtx.com/news-releases…

Nurix Therapeutics Presents Positive Results from Ongoing Clinical Trial of NX-5948 in Patients...

Objective response rate of 69.2% observed in heavily pretreated patient population including patients with BTK inhibitor resistance mutations Clinical responses in CLL patients were rapid and...

ir.nurixtx.com
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We are recruiting: ERC- and DFG-funded PhD positions in Tumor Biology (Kiel, Germany). We look forward to your application!
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Congratulations to all the authors on their great work!
Markus Damme@DammeMarkus
10 Jun 2024
More than happy to finally see our paper out in @NatureCellBio! We de-orphanized MFSD1 as a lysosomal dipeptide uniporter. Fantastic work of @Kathaschnatta, @OceaneGuelle, @AllUNeedIsLoew and Bruno Gasnier: nature.com/articles/s41556-0… so nice to see the structure of MFSD1&GLMP!
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Thank you!
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Acute degradation of RUVBL1 in transplanted PDAC tumors via the auxin-inducible degron (AID) system resulted in complete tumor regression in immunocompetent mice which was preceded by infiltration with CD3-positive immune cells.
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Thereby, targeting of RUVBL1/2 transforms PDAC into an immunologically “hot” tumor, responsive to immunotherapy. In summary, our work identified the MYC-RUVBL1/2 axis as a druggable vulnerability of MYC-driven cancer.
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Congratulations to @MV4_11, @NevenkaDudvars1 and the other contributing members of @_WolfLab and many thanks to our collaborators @MYCGyvers, @seyvos, @WiegeringLab, @DiefenbacherL, @GeorgGasteiger, Florian Erhard, Stefan Knapp and Dieter Saur.
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We investigated the possibility of targeting the prominent oncogene MYC via its binding partners. We prioritized MYC binding partners by genetic screens in PDAC cells in culture and in immunocompetent mice.
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RUVBL1/2 interacts directly with MYC and gets recruited to chromatin by MYC, where it is required to establish oncogenic and immune-evasive gene expression.
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While PDAC dependencies in cell culture followed public essentiality data of the @CancerDepMap portal, dependencies on MYC binding partners were reduced in vivo. Among the most essential MYC binding partners in vivo were RUVBL1 and RUVBL2 which form a AAA ATPase complex.
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