[BioRxiv] RBProximity-CLIP Enables Subcellular Mapping of RNA-Binding Protein Interactions at Nucleotide Resolution
https://doi.org/10.64898/2025.12.12.693770
#neurodegeneration #biorxiv #RNAbindingprotein
[BioRxiv] Native, full-length, refolding-assisted purification of TDP-43 compatible with BSL-2 safety regulations
https://doi.org/10.64898/2025.12.10.693404
#neurodegeneration #biorxiv #Dementia #ALS #RNAbindingprotein
[BioRxiv] RNA modulates FUS condensate assembly, dynamics, and aggregation through diverse molecular contacts
https://doi.org/10.64898/2025.12.13.694118
#neurodegeneration #biorxiv #phaseseparation #RNAbindingprotein #aggregate
[BioRxiv] ALS/FTD-associated TDP-43 mutations promote fragility of genes governing excitatory neurotransmission via topoisomerase IIβ impairment
https://doi.org/10.64898/2025.12.08.693088
#neurodegeneration #biorxiv #ALS #RNAbindingprotein #Dementia
[BioRxiv] Molecular Visualization of Neuronal TDP43 Pathology In Situ
https://doi.org/10.1101/2024.08.19.608477
#neurodegeneration #biorxiv #ALS #RNAbindingprotein
A schematic diagram showing two models of HIV-1 infection. Left panel (HIV-1 latency model): Under HIV-1 infection, upregulated RBM39 promotes m⁶A methylation of Tat RNA. This modification is recognized by YTHDC1, which subsequently recruits the RNA helicase DDX5 to degrade m⁶A-methylated Tat RNA. As a result, Tat RNA fails to undergo splicing and translation into functional Tat protein, thereby preventing activation of the HIV-1 LTR promoter and maintaining viral latency. Right panel (HIV-1 reactivation model): Treatment with indisulam induces degradation of RBM39. This abolishes the recognition of Tat RNA by YTHDC1 and its degradation by DDX5. Consequently, Tat RNA is efficiently translated into Tat protein, which activates the HIV-1 LTR promoter, leading to HIV-1 reactivation.
Latent HIV-1 resists current #reactivation therapies, hindering viral eradication. This study identifies #RNAbindingProtein RBM39 as a scaffold assembling an m⁶A-dependent RNA decay complex that degrades Tat transcripts, enforcing & maintaining #HIV1 latency @plosbiology.org 🧪 plos.io/4nRrHsO
A schematic diagram showing two models of HIV-1 infection. Left panel (HIV-1 latency model): Under HIV-1 infection, upregulated RBM39 promotes m⁶A methylation of Tat RNA. This modification is recognized by YTHDC1, which subsequently recruits the RNA helicase DDX5 to degrade m⁶A-methylated Tat RNA. As a result, Tat RNA fails to undergo splicing and translation into functional Tat protein, thereby preventing activation of the HIV-1 LTR promoter and maintaining viral latency. Right panel (HIV-1 reactivation model): Treatment with indisulam induces degradation of RBM39. This abolishes the recognition of Tat RNA by YTHDC1 and its degradation by DDX5. Consequently, Tat RNA is efficiently translated into Tat protein, which activates the HIV-1 LTR promoter, leading to HIV-1 reactivation.
Latent HIV-1 resists current #reactivation therapies, hindering viral eradication. This study identifies #RNAbindingProtein RBM39 as a scaffold assembling an m⁶A-dependent RNA decay complex that degrades Tat transcripts, enforcing & maintaining #HIV1 latency @plosbiology.org 🧪 plos.io/4nRrHsO
A schematic diagram showing two models of HIV-1 infection. Left panel (HIV-1 latency model): Under HIV-1 infection, upregulated RBM39 promotes m⁶A methylation of Tat RNA. This modification is recognized by YTHDC1, which subsequently recruits the RNA helicase DDX5 to degrade m⁶A-methylated Tat RNA. As a result, Tat RNA fails to undergo splicing and translation into functional Tat protein, thereby preventing activation of the HIV-1 LTR promoter and maintaining viral latency. Right panel (HIV-1 reactivation model): Treatment with indisulam induces degradation of RBM39. This abolishes the recognition of Tat RNA by YTHDC1 and its degradation by DDX5. Consequently, Tat RNA is efficiently translated into Tat protein, which activates the HIV-1 LTR promoter, leading to HIV-1 reactivation.
Latent HIV-1 resists current #reactivation therapies, hindering viral eradication. This study identifies #RNAbindingProtein RBM39 as a scaffold assembling an m⁶A-dependent RNA decay complex that degrades Tat transcripts, enforcing & maintaining #HIV1 latency @plosbiology.org 🧪 plos.io/4nRrHsO
AlphaFold model of the complex formed between HK2 and the SOX10 5′UTR (189–204 nts). The predicted RNA structure is shown in cyan, and HK2 protein is shown in green. HK2 residues and SOX10 mRNA nucleotides at the interaction interface are highlighted in red. Inset: schematic representation of the secondary structure of the SOX10 5′UTR (189–204 nts) predicted by Mfold, with the putative HK2-binding region (194–198 nts) marked in red.
Hexokinase 2 (HK2) is known for its metabolic role in #glycolysis. This study shows that it also functions as an #RNAbindingProtein that regulates mRNA translation, particularly of SOX10, promoting #melanoma cell proliferation independently of glycolysis @plosbiology.org 🧪 plos.io/3ViI1qL
AlphaFold model of the complex formed between HK2 and the SOX10 5′UTR (189–204 nts). The predicted RNA structure is shown in cyan, and HK2 protein is shown in green. HK2 residues and SOX10 mRNA nucleotides at the interaction interface are highlighted in red. Inset: schematic representation of the secondary structure of the SOX10 5′UTR (189–204 nts) predicted by Mfold, with the putative HK2-binding region (194–198 nts) marked in red.
Hexokinase 2 (HK2) is known for its metabolic role in #glycolysis. This study shows that it also functions as an #RNAbindingProtein that regulates mRNA translation, particularly of SOX10, promoting #melanoma cell proliferation independently of glycolysis @plosbiology.org 🧪 plos.io/3ViI1qL
AlphaFold model of the complex formed between HK2 and the SOX10 5′UTR (189–204 nts). The predicted RNA structure is shown in cyan, and HK2 protein is shown in green. HK2 residues and SOX10 mRNA nucleotides at the interaction interface are highlighted in red. Inset: schematic representation of the secondary structure of the SOX10 5′UTR (189–204 nts) predicted by Mfold, with the putative HK2-binding region (194–198 nts) marked in red.
Hexokinase 2 (HK2) is known for its metabolic role in #glycolysis. This study shows that it also functions as an #RNAbindingProtein that regulates mRNA translation, particularly of SOX10, promoting #melanoma cell proliferation independently of glycolysis @plosbiology.org 🧪 plos.io/3ViI1qL
RESEARCH PAPER: ELAV mediates circular RNA biogenesis in neurons
By Alfonso-Gonzalez et al.
➡️ https://tinyurl.com/gd352670
#circRNA #neuroscience #RNAbindingprotein #Drosophila #embryos #neurons #mRNA #introns #splicing
For the month of July get to know Amina, PhD student from the RBP ReguNet-MSCA Network. Amina joined Immagina in the beginning of last year and integrated the R&D team since 👩🔬🔬Learn more about her 👇
#employeespotlight #ribosome #RNAbindingprotein
RNA-binding proteins DND1 and NANOS3 cooperatively suppress the entry of germ cell lineage.
https://pubmed.ncbi.nlm.nih.gov/40410171/
#neurodegeneration #RNAbindingprotein
Functional prediction of DNA/RNA-binding proteins by deep learning from gene expression correlations
www.biorxiv.org/content/10.1101/2025.03....
#neurodegeneration #RNAbindingprotein
Small molecule inhibitors of hnRNPA2B1-RNA interactions reveal a predictable sorting of RNA subsets into extracellular vesicles - PubMed
https://pubmed.ncbi.nlm.nih.gov/40103230/
#neurodegeneration #RNAbindingprotein #APP
Profiling local translatomes and RNA binding proteins of somatosensory neurons reveals specializations of individual axons | bioRxiv
www.biorxiv.org/content/10.1101/2025.02....
#neurodegeneration #ALS #RNAbindingprotein
This looks like a very interesting #preprint @biorxiv-cellbio.bsky.social from Christine Mayr lab:
"The FXR1 network acts as signaling scaffold for actomyosin remodeling"
🧬#RNA #mRNA #RNABindingProtein #microscopy 🔬
www.biorxiv.org/content/10.1...
