Search bioRxiv⌕ Search

Biology subjects

Samuel, C.

Publications and source records attributed to Samuel, C..

3 recordsLinked to original sources

Predicting conformational changes induced by biomolecular interactions

Biomolecular interactions trigger structural changes of protein complexes essential for cellular signaling, regulation, and drug action. Modern co-folding models can now generate detailed structures of multi-component complexes directly from sequence. However, recent evaluations reveal that they frequently fail to capture specific conformational states induced by a ligand or partner. Here, we show that explicitly modeling the structural transition from an unbound to a bound state, rather than generating the bound complex alone, better resolves these interaction-induced states. Our generative learning framework, K-Fold, transforms independently predicted unbound component priors into an assembled complex through an ultrafast diffusion bridge, operating entirely without multiple sequence alignments. By eliminating co-evolutionary dependencies, K-Fold accurately recovers non-coevolved interfaces in antibody-antigen and targeted-degrader complexes, as well as ligand-directed regulatory states in GPCRs and kinases. Furthermore, by coupling this diffusion bridge with diverse monomeric equilibrium ensembles, K-Fold provides a computationally tractable foundation for sampling complex multi-state landscapes without retraining. These results demonstrate that formulating molecular assembly as an explicit structural transition moves structure prediction beyond static geometries toward capturing biomolecular dynamics.

molecular biology↗

Defining the RNA Modification Landscape of Multiple Myeloma Reveals METTL3-Dependent m6A Regulation of NEAT1

RNA modifications play critical roles in gene regulation. N6-methyladenosine (m6A) is the most abundant modification on mRNA and long noncoding RNA (lncRNA) and regulates RNA processing, stability, and translation. RNA modifications are not well characterized in multiple myeloma (MM), a plasma cell malignancy characterized by relapse and disease progression, and the contribution of m6A-modified lncRNAs to the disease remains unclear. Here, we define the RNA modification landscape of MM by combining mass spectrometry, Nanopore Direct RNA sequencing, and methylated RNA immunoprecipitation sequencing. We identify 20 RNA modification types and > 15,000 m6A sites, including sites on 2,398 lncRNAs. Among these, we validate m6A sites on the paraspeckle-associated lncRNA NEAT1. Functional studies reveal that NEAT1 expression is regulated by the methyltransferase METTL3 and site-specific demethylation of a NEAT1 m6A site reduces MM cell viability. Single-cell RNA sequencing shows consistent NEAT1 enrichment in malignant plasma cells but minimal expression in healthy cells. These findings identify m6A-modified lncRNAs as key regulators of MM biology and establish NEAT1 as an epitranscriptomically controlled driver of MM cell survival.

cancer biology↗

Topical GZ21T inhibits the growth of actinic keratoses in a UVB induced model of skin carcinogenesis

Actinic keratoses (AKs) are premalignant intraepidermal neoplasms that occur as a result of cumulative sun damage. AKs commonly relapse, and up to 16% undergo malignant transformation into cutaneous squamous cell carcinoma (cSCC). There is a need for novel therapies that reduce the quantity and surface area of AKs as well as prevent malignant transformation to cSCCs. We recently showed that GZ17-6.02, an anti-cancer agent composed of curcumin, haramine, and isovanillin, inhibited the growth of H297.T cells. The present study evaluated the efficacy of a novel topical formulation of GZ17-6.02, known as GZ21T, in a murine model of AK generated by exposing SKH1 mice to ultraviolet irradiation. Treatment of mice with topical GZ21T inhibited the growth of AKs by decreasing both lesion count (p=.028) and surface area occupied by tumor (p=.026). GZ21T also suppressed the progression of AKs to cSCC by decreasing the count (p=.047) and surface area (p=.049) of lesions more likely to represent cSCC. RNA sequencing and proteomic analyses revealed that GZ21T suppressed several pathways, including MAPK (p=.026), Pi3K-Akt (p=.028), HIF-1 (p=.030), Wnt (p=.031), insulin (p=.011), and ErbB (p=.006) signaling. GZ21T also upregulated the autophagy-promoting protein AMPK, while suppressing proteins such as PD-L1, glutaminase, pAkt1 S473, and eEF2K. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=200 SRC="FIGDIR/small/506864v1_ufig1.gif" ALT="Figure 1"> View larger version (44K): org.highwire.dtl.DTLVardef@1254e6corg.highwire.dtl.DTLVardef@3fd190org.highwire.dtl.DTLVardef@1d75eb5org.highwire.dtl.DTLVardef@8afc97_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗