Sepulveda Yañez, Julieta Haydee

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Nombre completo

Sepulveda Yañez, Julieta Haydee

Afiliación principal

Facultad de Ciencias de la Salud

julieta.sepulveda@umag.cl

ORCID

0000-0001-6354-3609

Jerarquía académica

Prof. Asociado/a

Línea de investigación

Bienestar y Desarrollo Humano

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Publicaciones

Mostrando 1 - 10 de 13

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DOI 10.1093/bib/bbae275
Peptide-based drug discovery through artificial intelligence: towards an autonomous design of therapeutic peptides
2024-06-10
Goles, Montserrat
;
Daza, Anamaria
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Cabas-Mora, Gabriel
;
Sarmiento-Varon, Lindybeth
;
Sepulveda-Yanez, Julieta
;
Anvari-Kazemabad, Hoda
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Davari, Mehdi D.
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Uribe-Paredes, Roberto
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Olivera-Nappa, Alvaro
;
Navarrete, Marcelo A.
With their diverse biological activities, peptides are promising candidates for therapeutic applications, showing antimicrobial, antitumour and hormonal signalling capabilities. Despite their advantages, therapeutic peptides face challenges such as short half-life, limited oral bioavailability and susceptibility to plasma degradation. The rise of computational tools and artificial intelligence (AI) in peptide research has spurred the development of advanced methodologies and databases that are pivotal in the exploration of these complex macromolecules. This perspective delves into integrating AI in peptide development, encompassing classifier methods, predictive systems and the avant-garde design facilitated by deep-generative models like generative adversarial networks and variational autoencoders. There are still challenges, such as the need for processing optimization and careful validation of predictive models. This work outlines traditional strategies for machine learning model construction and training techniques and proposes a comprehensive AI-assisted peptide design and validation pipeline. The evolving landscape of peptide design using AI is emphasized, showcasing the practicality of these methods in expediting the development and discovery of novel peptides within the context of peptide-based drug discovery.
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DOI 10.1093/bib/bbae275
Peptide-based drug discovery through artificial intelligence: towards an autonomous design of therapeutic peptides
2024-06-10
Goles, Montserrat
;
Daza, Anamaria
;
Cabas-Mora, Gabriel
;
Sarmiento-Varon, Lindybeth
;
Sepulveda-Yanez, Julieta
;
Anvari-Kazemabad, Hoda
;
Davari, Mehdi D.
;
Uribe-Paredes, Roberto
;
Olivera-Nappa, Alvaro
;
Navarrete, Marcelo A.
With their diverse biological activities, peptides are promising candidates for therapeutic applications, showing antimicrobial, antitumour and hormonal signalling capabilities. Despite their advantages, therapeutic peptides face challenges such as short half-life, limited oral bioavailability and susceptibility to plasma degradation. The rise of computational tools and artificial intelligence (AI) in peptide research has spurred the development of advanced methodologies and databases that are pivotal in the exploration of these complex macromolecules. This perspective delves into integrating AI in peptide development, encompassing classifier methods, predictive systems and the avant-garde design facilitated by deep-generative models like generative adversarial networks and variational autoencoders. There are still challenges, such as the need for processing optimization and careful validation of predictive models. This work outlines traditional strategies for machine learning model construction and training techniques and proposes a comprehensive AI-assisted peptide design and validation pipeline. The evolving landscape of peptide design using AI is emphasized, showcasing the practicality of these methods in expediting the development and discovery of novel peptides within the context of peptide-based drug discovery.
Scopus© Citations 101 30
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DOI 10.1182/blood-2022-168211
Unbiased NGS Approach for IGHV Mutational Status, Clonal Space and Immune Repertoire Assessment in Chronic Lymphocytic Leukemia
2022-11-15
Gonzalez-Puelma, Jorge
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Opezo, Pablo
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Alvarez-Ojeda, Hermy
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Sepulveda Yañez, Julieta Haydee
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Elena Marquez, Maria
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Alvarez-Saravia, Diego
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Cardemil, Daniela
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Navarrete Signorile, Marcelo Alejandro
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Uribe Paredes, Roberto Alex
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Torres-Almonacid, Jorge
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DOI 10.1182/blood-2022-169429
Autonomous BCR Signaling and Genetic Aberrations in CLL-Phenotype Monoclonal B Lymphocytosis in Siblings of CLL Patients
2022-11-15
Sepulveda Yañez, Julieta Haydee
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Quinten, Edwin
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Koning, Marvyn T.
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Eken, Janneke A.
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Pfeifer, Dietmar
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De Groen, Ruben A. L.
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Alvarez Saravia, Diego
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Agathangelidis, Andreas
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van Bergen, Cornelis A. M.
;
Stamatopoulos, Kostas
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DOI 10.1182/blood-2022-168211
Unbiased NGS Approach for IGHV Mutational Status, Clonal Space and Immune Repertoire Assessment in Chronic Lymphocytic Leukemia
2022-11-15
Gonzalez-Puelma, Jorge
;
Opezo, Pablo
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Alvarez-Ojeda, Hermy
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Sepulveda Yañez, Julieta Haydee
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Elena Marquez, Maria
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Alvarez-Saravia, Diego
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Cardemil, Daniela
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Navarrete Signorile, Marcelo Alejandro
;
Uribe Paredes, Roberto Alex
;
Torres-Almonacid, Jorge
5
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DOI 10.1182/blood-2022-169429
Autonomous BCR Signaling and Genetic Aberrations in CLL-Phenotype Monoclonal B Lymphocytosis in Siblings of CLL Patients
2022-11-15
Sepulveda Yañez, Julieta Haydee
;
Quinten, Edwin
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Koning, Marvyn T.
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Eken, Janneke A.
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Pfeifer, Dietmar
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De Groen, Ruben A. L.
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Alvarez Saravia, Diego
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Agathangelidis, Andreas
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van Bergen, Cornelis A. M.
;
Stamatopoulos, Kostas
7
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DOI 10.3389/fimmu.2021.807015
Tandem Substitutions in Somatic Hypermutation
2022-01-07
Sepulveda Yañez, Julieta Haydee
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Alvarez Saravia, Diego
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Pilzecker, Bas
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van Schouwenburg, Pauline A.
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van den Burg, Mirjam
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Veelken, Hendrik
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Navarrete Signorile, Marcelo Alejandro
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Jacobs, Heinz
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Koning, Marvyn T.
Upon antigen recognition, activation-induced cytosine deaminase initiates affinity maturation of the B-cell receptor by somatic hypermutation (SHM) through error-prone DNA repair pathways. SHM typically creates single nucleotide substitutions, but tandem substitutions may also occur. We investigated incidence and sequence context of tandem substitutions by massive parallel sequencing of V(D)J repertoires in healthy human donors. Mutation patterns were congruent with SHM-derived single nucleotide mutations, delineating initiation of the tandem substitution by AID. Tandem substitutions comprised 5,7% of AID-induced mutations. The majority of tandem substitutions represents single nucleotide juxtalocations of directly adjacent sequences. These observations were confirmed in an independent cohort of healthy donors. We propose a model where tandem substitutions are predominantly generated by translesion synthesis across an apyramidinic site that is typically created by UNG. During replication, apyrimidinic sites transiently adapt an extruded configuration, causing skipping of the extruded base. Consequent strand decontraction leads to the juxtalocation, after which exonucleases repair the apyramidinic site and any directly adjacent mismatched base pairs. The mismatch repair pathway appears to account for the remainder of tandem substitutions. Tandem substitutions may enhance affinity maturation and expedite the adaptive immune response by overcoming amino acid codon degeneracies or mutating two adjacent amino acid residues simultaneously.
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DOI 10.3389/fimmu.2021.807015
Tandem Substitutions in Somatic Hypermutation
2022-01-07
Sepulveda Yañez, Julieta Haydee
;
Alvarez Saravia, Diego
;
Pilzecker, Bas
;
van Schouwenburg, Pauline A.
;
van den Burg, Mirjam
;
Veelken, Hendrik
;
Navarrete Signorile, Marcelo Alejandro
;
Jacobs, Heinz
;
Koning, Marvyn T.
Upon antigen recognition, activation-induced cytosine deaminase initiates affinity maturation of the B-cell receptor by somatic hypermutation (SHM) through error-prone DNA repair pathways. SHM typically creates single nucleotide substitutions, but tandem substitutions may also occur. We investigated incidence and sequence context of tandem substitutions by massive parallel sequencing of V(D)J repertoires in healthy human donors. Mutation patterns were congruent with SHM-derived single nucleotide mutations, delineating initiation of the tandem substitution by AID. Tandem substitutions comprised 5,7% of AID-induced mutations. The majority of tandem substitutions represents single nucleotide juxtalocations of directly adjacent sequences. These observations were confirmed in an independent cohort of healthy donors. We propose a model where tandem substitutions are predominantly generated by translesion synthesis across an apyramidinic site that is typically created by UNG. During replication, apyrimidinic sites transiently adapt an extruded configuration, causing skipping of the extruded base. Consequent strand decontraction leads to the juxtalocation, after which exonucleases repair the apyramidinic site and any directly adjacent mismatched base pairs. The mismatch repair pathway appears to account for the remainder of tandem substitutions. Tandem substitutions may enhance affinity maturation and expedite the adaptive immune response by overcoming amino acid codon degeneracies or mutating two adjacent amino acid residues simultaneously.
Scopus© Citations 3
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DOI 10.3390/ijms222313015
Integration of Mutational Signature Analysis with 3D Chromatin Data Unveils Differential AID-Related Mutagenesis in Indolent Lymphomas
2021-12
Sepulveda Yañez, Julieta Haydee
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Alvarez-Saravia, Diego
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Fernández Goycoolea, José Antonio
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Aldridge, Jacqueline
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van Bergen, Cornelis A. M.
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Posthuma, Ward
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Uribe Paredes, Roberto Alex
;
Veelken, Hendrik
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Navarrete Signorile, Marcelo Alejandro
Activation-induced deaminase (AID) is required for somatic hypermutation in immunoglobulin genes, but also induces off-target mutations. Follicular lymphoma (FL) and chronic lymphocytic leukemia (CLL), the most frequent types of indolent B-cell tumors, are exposed to AID activity during lymphomagenesis. We designed a workflow integrating de novo mutational signatures extraction and fitting of COSMIC (Catalogue Of Somatic Mutations In Cancer) signatures, with tridimensional chromatin conformation data (Hi-C). We applied the workflow to exome sequencing data from lymphoma samples. In 33 FL and 30 CLL samples, 42% and 34% of the contextual mutations could be traced to a known AID motif. We demonstrate that both CLL and FL share mutational processes dominated by spontaneous deamination, failures in DNA repair, and AID activity. The processes had equiproportional distribution across active and nonactive chromatin compartments in CLL. In contrast, canonical AID activity and failures in DNA repair pathways in FL were significantly higher within the active chromatin compartment. Analysis of DNA repair genes revealed a higher prevalence of base excision repair gene mutations (p = 0.02) in FL than CLL. These data indicate that AID activity drives the genetic landscapes of FL and CLL. However, the final result of AID-induced mutagenesis differs between these lymphomas depending on chromatin compartmentalization and mutations in DNA repair pathways.
Scopus© Citations 2 4
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DOI 10.1182/blood-2021-150475
"Snapshotting" Somatic Hypermutation in Single Follicular Lymphoma Cells
2021-11-23
Sepulveda Yañez, Julieta Haydee
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Alvarez-Saravia, Diego
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Quinten, Edwin
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Menafra, Roberta
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Kloet, Susan L.
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Monajemi, Ramin
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Kielbasa, Szymon M.
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Navarrete Signorile, Marcelo Alejandro
;
van Bergen, Cornelis A. M.
;
Veelken, Hendrik
1

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