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Satpathy, S.

Publications and source records attributed to Satpathy, S..

17 recordsLinked to original sources

Integrated coding-noncoding genome annotation expands single-cell transcriptomic discovery and identifies clinically relevant noncoding RNAs in multiple myeloma

Although the human genome encodes a vast repertoire of noncoding RNAs that regulate gene expression, the noncoding genome remains underexplored due to technical challenges. Specifically, during transcriptomic sequencing data alignment, the overlap between noncoding and coding loci can create ambiguous read alignments that are subsequently discarded from downstream analysis. For this reason, most of the noncoding genome is excluded from standard genomic annotations used for sequencing alignment. To address this challenge and enable concurrent profiling of the coding and noncoding transcriptome, we systematically integrated standard coding (GENCODE) and noncoding (LncBook) genome annotations, preserving coding gene annotations and removing overlapping noncoding regions. The resulting integrated genome annotation expanded the number of annotated noncoding genes from 40,785 to 138,296 while preserving all coding genes and reducing ambiguous read assignment. To evaluate the utility of our integrated genome annotation for uncovering novel, biologically relevant noncoding RNAs (ncRNAs), we realigned CD138-positive bulk RNA-seq (N = 942) and CD138-negative single-cell RNA-seq (N = 478) data from the MMRF CoMMpass study, generating a comprehensive coding-noncoding atlas of the myeloma bone marrow microenvironment with noncoding genes representing 51% of highly variable genes and displaying significant cell type specificity. Tumor expression profiling based on this integrated profiling identified 15 clusters, including two enriched for amp(1q21) or t(4;14) and associated with shorter progression-free survival (PFS). Differential expression and systematic filtering yielded 19 candidate high-risk ncRNAs, including previously uncharacterized ENSG00000310209, which was associated with poor PFS (HR = 1.141, P = 0.0025), increased IRF4 activity, Wnt pathway activation, CCL5 signaling, and the accumulation of anergic-like CD8+ T cells. These findings establish integrated coding-noncoding analysis as a strategic approach for discovering functional ncRNAs from transcriptomic sequencing data.

cancer biology↗

Single-cell profiling of innate and adaptive immune dysregulation in Long COVID

The COVID-19 pandemic has infected more than 778 million people worldwide. Roughly 7% of these patients progress to Long COVID (LC), suffering from persistent symptoms and cognitive impairment well past the acute stage. As the mechanisms of LC remain elusive, we utilized single-cell profiling (SCP) on 156,478 peripheral blood mononuclear cells (PBMCs) from 20 LC patients and 18 recovered controls (RC) to characterize the disease-associated immune dysregulation. Comparative analysis of LC and RC profiles revealed cellular heterogeneity along with differential abundances across B, T, and myeloid cell compartments. The focused analysis on the B-cell compartment showed that naive B cells in the LC exhibit elevated IL4R expression and BCR signaling, indicative of sustained antigen exposure and aberrant chronic activation. Concurrently, monocytes adopted heightened interferon signaling and enhanced migratory states, culminating into impaired myeloid differentiation. Furthermore, the T-cell compartment exhibited a functional dichotomy, maintaining sustained quiescence in the central memory compartment while displaying chronic exhaustion within effector memory populations. This dysregulation of effector immunity extended to the NK compartment, where terminally differentiated cells exhibited increased cytotoxicity yet compromised regulatory function, potentially contributing to poor viral clearance. Cellular communication analysis further supports this NK cell dysfunction that is likely driven by galectin and prostaglandin signaling involving monocytes and B cells. We stratified LC patients into mild and severe groups based on symptom and cognitive severity, identifying a distinct immune signature where severe disease is linked to chronic AP-1-mediated inflammation in NK cells and CD14+ monocytes. In contrast, patients with mild symptoms retain functionally competent NK cells with significantly lower exhaustion and apoptosis scores. Collectively, these insights into persistent immune remodeling provide a crucial framework for future biomarker discovery and the development of targeted therapeutic strategies. Abstract (Short)COVID-19 has affected >778 million worldwide, with [~]7% developing Long COVID (LC), characterized by persistent symptoms and cognitive impairment. The mechanisms of LC remain elusive; we utilized single-cell profiling on 156,478 peripheral blood mononuclear cells from LC and recovered controls. Comparative analysis revealed cellular heterogeneity and differential abundance across multiple immune compartments. B-cells exhibited hallmarks of sustained antigen exposure and aberrant activation. Concurrently, monocytes adopted heightened interferon signaling, enhanced migratory states, and impaired differentiation. T-cells exhibited chronic exhaustion within the effector memory populations. Dysregulated effector immunity extended to NK, with increased expression of cytotoxic genes yet compromised regulatory function, potentially contributing to viral clearance. LC patients with severe symptoms showed enhanced AP-1-mediated inflammation in NK cells and CD14+ monocytes, whereas mild cases had fitter NK cells with significantly lower exhaustion and apoptosis. Collectively, these insights provide a framework for biomarker discovery and the development of targeted LC therapeutic strategies.

genomics↗

Patient-derived organoid xenografts reveal the multifaceted role of the lncRNA MALAT1 in breast cancer progression

Long non-coding RNAs (lncRNAs) have emerged as key regulators of tumor biology, however, thus far none have translated to cancer therapies. The lncRNA MALAT1 is overexpressed in more than 20 cancers, including breast cancer and has been shown to function via various mechanisms in a context-dependent manner, in 2D cell lines and mouse models. However, its functional role and therapeutic potential have not been evaluated in clinically relevant patient-derived models. We investigated the therapeutic potential of MALAT1-targeting antisense oligonucleotides (ASOs) for breast cancer, using clinically relevant 3D human patient-derived organoids (PDOs) and PDO-xenograft (PDO-X) models. We systematically evaluated the efficiency of MALAT1-targeting ASOs using a biobank of 28 PDO models. Across three independent PDO-X models of triple negative breast cancer (TNBC), MALAT1 depletion reproducibly drove widespread alternative splicing changes across all event types, with an enrichment of intron retention. Differentially spliced transcripts were enriched for targets of shared cancer-associated transcription factors, and MALAT1 knockdown specifically altered the relative abundance of previously unannotated splicing isoforms. Beyond tumor-intrinsic effects, tumor-specific MALAT1 depletion induced a consistent reduction in macrophage-associated gene signatures and reduced lung metastatic burden. Our data defines MALAT1s multifaceted role in TNBC, coordinating alternative splicing, tumor-stroma crosstalk, and metastatic progression. Our study provides strong preclinical evidence supporting MALAT1-targeted ASO therapy and establishes PDO-X models as a clinically relevant platform for functional interrogation of TNBC therapies. SignificanceUsing clinically relevant human PDO-X models, we show that MALAT1 influences alternative splicing, metastatic potential and the tumor microenvironment. These data support the potential of oncogenic lncRNA MALAT1 as a therapeutic target.

cancer biology↗

Spatial multi-omics of multiple myeloma uncovers niche-dependent pro-myeloma and immunosuppressive signaling in the bone marrow and extramedullary lesions

Multiple myeloma (MM) is a plasma cell malignancy shaped by dynamic interactions between MM cells and non-malignant cells in the immune microenvironment. To spatially profile the influence of cellular context on MM and immune cell expression, we developed a multimodal framework integrating 10x Genomics Visium HD, 10x Genomics Xenium, and clinically annotated single-cell RNA (scRNA-seq) sequencing datasets. Visium HD enabled unbiased, whole transcriptome, spatial discovery at 16 {micro}m resolution, Xenium provided orthogonal validation at single-cell resolution, and scRNA-seq extended findings by mapping spatial labels and leveraging the greater sequencing depth. We developed a custom framework for cell type annotation within Visium HD spatial bins. Our approach enabled identification of plasma cell-dense niches enriched for non-canonical Wnt signaling, associated with gene expression supporting cell adhesion mediated drug resistance, inferior progression-free survival, and extramedullary lesions. Immune cells within these neighborhoods exhibited suppressed transcriptional states, including increased inhibitory receptor expression such as LAG3. Utilizing the niche-driven transcriptional states in MM and immune cells, we were able to develop a 15-gene signature independently predictive of progression free survival (HR = 2.00, p < 0.0001). Collectively, this study demonstrates the potential of integrated spatial and single-cell transcriptomics to define niche-specific programs supporting MM progression.

cancer biology↗

Microscaled Cell Surface Proteomics for Cryo-preserved and Tissue Samples

Cell surface proteins (CSPs) regulate key cellular functions and represent valuable targets for diagnostics and therapeutics. Despite advances in proteomic workflows, CSP analysis from cryopreserved or low-input clinical samples remains limited by technical constraints, including reduced membrane integrity, inefficient labeling, and high background. To address these challenges, we optimized and benchmarked two complementary surface enrichment strategies compatible with low-input applications (fewer than 1 million cells) and real-world sample types, including fresh, viably cryopreserved, and dissociated solid tissues. We systematically compared oxidation-based N-glycoprotein capture and WGA-HRP-mediated proximity labeling across a range of input amounts using both solid tumor (A549) and hematologic cancer (KMS-12-BM) cell lines. The N-glycopeptide method yielded superior specificity in low-input contexts, while WGA-HRP captured complementary CSP subsets. Together, the methods identified more than 700 CSPs, with approximately 175 unique identifications per protocol. Both workflows detected dynamic EGFR internalization following EGF stimulation and maintained high reproducibility (Pearson correlation greater than 0.9) between fresh and cryopreserved preparations. To extend these findings to tissue-derived samples, we optimized dissociation protocols for healthy endometrium and applied the N-glycopeptide method to cryopreserved dissociated endometrium from three healthy donors. Enzymatic dissociation enabled accurate CSP profiling from fewer than 1 to 2 million cells. This study provides a systematic comparison of two leading surface proteomics approaches, validates their performance on cryopreserved and low-input specimens, and demonstrates applicability to clinically relevant tissues. Our optimized workflows enable robust surfaceome characterization in translational settings where sample quantity and preservation methods are often limiting, opening new avenues for biomarker discovery and patient stratification.

cell biology↗

Longitudinal multi-omic profiling uncovers immune escape and predictors of response in multiple myeloma

Multiple myeloma (MM) is an incurable malignancy of clonally expanded plasma cells shaped by complex interactions with the immune microenvironment. To investigate immune factors driving treatment response and resistance, we conducted multi-omics profiling including CD138neg single-cell RNA sequencing of 243 bone marrow samples from 102 patients (631,226 cells) and CD138pos bulk RNA and whole-genome sequencing from 209 samples. Longitudinal analyses revealed that interferon gamma signaling impairs T cell memory after autologous stem cell transplant, while naive B cell abundance and immunoglobulin diversity correlated with improved progression-free survival (HR = 0.48, p = 2.3e-4). At disease progression, MM cells upregulated cancer-testis antigens and immune effector genes, with concurrent B cell depletion, enrichment of myeloid-derived suppressor cell genes in monocytes, and T cell exhaustion. These findings highlight dynamic immune-tumor interactions, identifying naive B cell reconstitution as a biomarker of durable response, and cancer-testis antigens as potential targets for high-risk disease at progression. Statement of SignificanceLongitudinal profiling of multiple myeloma and the immune microenvironment revealed dynamic immune-tumor interactions across the disease course. Dysfunctional CD8 T cells limited memory formation post-transplant, while naive B recovery associated with sustained treatment response. At progression, cancer-testis antigen expression associated with immunosuppression, revealing novel mechanisms of immune escape.

cancer biology↗

High-throughput proteomic and phosphoproteomic analysis of formalin-fixed paraffin-embedded tissue

Formalin-fixed, paraffin-embedded (FFPE) patient tissues are a valuable resource for proteomic studies with the potential to associate the derived molecular insights with clinical annotations and outcomes. Here we present an optimized, partially automated workflow for FFPE proteomics combining pathology-guided macro-dissection, Adaptive Focused Acoustics (AFA) sonication for lysis and decrosslinking, S-Trap digestion to peptides, and liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis using Orbitrap, Astral or timsTOF HT instrumentation. The workflow enables analysis of up to 96 dissected FFPE tissue samples or 10 {micro}m scrolls, identifying 8,000-10,000 unique proteins per sample with median CVs <20%. Key optimizations include improved tissue lysis strategies, protein quantification for normalization, and peptide cleanup prior to LC-MS/MS analysis. Application to lung adenocarcinoma (LUAD) FFPE blocks confirms the platforms effectiveness in processing complex, clinically relevant samples, achieving deep proteome coverage and quantitative robustness comparable to TMT-based methods. Using the newly released Orbitrap Astral with short, 24-minute gradients, the workflow identifies up to [~]10,000 unique proteins and [~]11,000 localized phosphosites in LUAD FFPE tissue. This high-throughput, scalable workflow advances biomarker discovery and proteomic research in archival tissue samples.

systems biology↗

Single-cell analysis of pediatric acute myeloid leukemia samples uncovers treatment-resistant stem and mast cells

Pediatric acute myeloid leukemia (pAML) is a heterogeneous malignancy driven by diverse cytogenetic mutations. While risk stratification improved by identifying cytogenetic lesions, prognostication remains inadequate with 30% of standard-risk patients experiencing relapse within 5 years. Single-cell RNA sequencing (scRNAseq) enabled the interrogation of malignant cell heterogeneity in pAML and characterization of the immune microenvironment. Herein we report the largest pAML scRNAseq analysis to date with 708,285 cells from 164 bone marrow biopsies of 95 patients and 11 healthy controls. We uncovered treatment-resistant (TR) subtypes of pAML specific to RUNX1-RUNX1T1, FLT3-ITD, and CBFB-MYH11 patients. The enrichment of TR subtype gene signatures on the TARGET pAML data supported an association with significantly poor outcomes. Intriguingly, in addition to leukemic stem cells, we identified mast cell-like pAML associated with treatment resistance and poor outcomes. Together, immature and mature pAML subtypes are promising biomarkers for identifying patients at increased risk of relapse within cytogenetic categories.

cancer biology↗

A single-cell atlas characterizes dysregulation of the bone marrow immune microenvironment associated with outcomes in multiple myeloma

Multiple Myeloma (MM) remains incurable despite advances in treatment options. Although tumor subtypes and specific DNA abnormalities are linked to worse prognosis, the impact of immune dysfunction on disease emergence and/or treatment sensitivity remains unclear. We established a harmonized consortium to generate an Immune Atlas of MM aimed at informing disease etiology, risk stratification, and potential therapeutic strategies. We generated a transcriptome profile of 1,149,344 single cells from the bone marrow of 263 newly diagnosed patients enrolled in the CoMMpass study and characterized immune and hematopoietic cell populations. Associating cell abundances and gene expression with disease progression revealed the presence of a proinflammatory immune senescence-associated secretory phenotype in rapidly progressing patients. Furthermore, signaling analyses suggested active intercellular communication involving APRIL-BCMA, potentially promoting tumor growth and survival. Finally, we demonstrate that integrating immune cell levels with genetic information can significantly improve patient stratification.

genomics↗

A systems-scale, integrated view of the ubiquitylation site occupancy and dynamics

Ubiquitylation regulates virtually all proteins and biological processes in a cell. However, the global site-specific occupancy (stoichiometry) and turnover rate of ubiquitylation have never been quantified. Here, we present the first integrated picture of ubiquitylation site occupancy and half-life. Ubiquitylation occupancy spans four orders of magnitude, but the median ubiquitylation site occupancy is three orders of magnitude lower than that of phosphorylation. The occupancy, turnover rate, and the regulation of sites by proteasome inhibitors show strong interrelationships. These properties can discriminate signaling-relevant sites from the sites involved in proteasomal degradation. The sites strongly upregulated by proteasome inhibitors have a longer half-life, and the half-life increases with increasing protein length. Importantly, a previously unknown surveillance mechanism rapidly deubiquitylates all ubiquitin-specific E1 and E2 enzymes and protects them against bystander ubiquitylation accumulation. This work reveals general principles of ubiquitylation-dependent governance and offers conceptual insights into the dynamic regulation of the cell. HighlightsO_LIUbiquitylation site occupancy is 3 orders of magnitude lower than phosphorylation C_LIO_LIThe highest 80% and the lowest 20% occupancy sites have distinct properties C_LIO_LIHigh occupancy sites are concentrated in the cytoplasmic domains of SLC proteins C_LIO_LIA dedicated mechanism prevevents ubiquitylation accumulation in E1s and E2s C_LI

biochemistry↗

MONTE enables serial immunopeptidome, ubiquitylome, proteome, phosphoproteome, acetylome analyses of sample-limited tissues

Serial multiomic analyses of proteome, phosphoproteome and acetylome provides functional insights into disease pathology and drug effects while conserving precious human material. To date, ubiquitylome and HLA peptidome analyses have required separate samples for parallel processing each using distinct protocols. Here we present MONTE, a highly-sensitive multi-omic native tissue enrichment workflow that enables serial, deepscale analysis of HLA-I and HLA-II immunopeptidome, ubiquitylome, proteome, phosphoproteome and acetylome from the same tissue samples. We demonstrate the capabilities of MONTE in a proof-of-concept study of primary patient lung adenocarcinoma(LUAD) tumors. Depth of coverage and quantitative precision at each of the omes is not compromised by serialization, and the addition of HLA immunopeptidomics enables identification of putative immunotherapeutic targets such as cancer/testis antigens and neoantigens. MONTE can provide insights into disease-specific changes in antigen presentation, protein expression, protein degradation, cell signaling, cross-talk and epigenetic pathways involved in disease pathology and treatment.

cancer biology↗

Automating UbiFast for High-throughput and Multiplexed Ubiquitin Enrichment

Robust methods for deep-scale enrichment and site-specific identification of ubiquitylation sites is necessary for characterizing the myriad roles of protein ubiquitylation. To this end we previously developed UbiFast, a sensitive method for highly multiplexed ubiquitylation profiling where K-{varepsilon}-GG peptides are enriched with anti-K-{varepsilon}-GG antibody and labeled on-antibody with isobaric labeling reagents for sample multiplexing. Here, we present robotic automation of the UbiFast method using a magnetic bead-conjugated K-{varepsilon}-GG antibody (mK-{varepsilon}-GG) and a magnetic particle processor. We report the identification of [~]20,000 ubiquitylation sites from a TMT10-plex with 500 g input per sample processed in [~]2 hours. Automation of the UbiFast method greatly increased the number of identified and quantified ubiquitylation sites, improved reproducibility and significantly reduced processing time. The workflow enables processing of up to 96 samples in a single day making it suitable to study ubiquitylation in large sample sets. Here we demonstrate the applicability of this method to profile small amounts of tissue using breast cancer patient-derived xenograft (PDX) tissue samples.

biochemistry↗

Highly multiplexed quantitative phosphosite assay for biology and preclinical studies

Reliable methods to quantify dynamic signaling changes across diverse pathways are needed to better understand the effects of disease and drug-treatment in cells and tissues but are presently lacking. Here we present SigPath, a targeted mass spectrometry (MS) assay that measures 284 phosphosites in 200 phosphoproteins of biological interest. SigPath probes a broad swath of signaling biology with high throughput and quantitative precision. We applied the assay to investigate changes in phospho-signaling in drug-treated cancer cell lines, breast cancer preclinical models and human medulloblastoma tumors. In addition to validating previous findings, SigPath detected and quantified a large number of differentially regulated phosphosites newly associated with disease models and human tumors at baseline or with drug perturbation. Our results highlight the potential of SigPath to monitor phosphoproteomic signaling events and to nominate mechanistic hypotheses regarding oncogenesis, response and resistance to therapy.

cancer biology↗

Antioxidant enriched fraction from Pueraria tuberosa alleviates ovariectomized-induced osteoporosis in rats, and inhibits growth of breast and ovarian cancer cell lines in vitro

Pueraria tuberosa (P. tuberosa), known as Indian Kudzu belongs to family Fabaceae and it is solicited as "Rasayana" drugs in Ayurveda. In the present study, we analyzed the efficacy an antioxidant enriched fraction (AEF) from the tuber extract of P. tuberosa against menopausal osteoporosis and breast and ovarian cancer cell lines. The AEF from P. tuberosa was identified by determining phenolic composition (total phenolic and flavonoid amount). Antioxidant property (in vitro assays) was also carried out followed by analysis of the AEF for its antiosteoporotic and anticancer potentials. Antiosteoporotic activity of AEF was investigated in ovariectomy-induced osteoporosis in rats and in vitro anticancer activity by MTT assay. Also, the GC/MS analysis of AEF was performed to determine various phytoconstituents. A docking analysis was performed to verify the interaction of bioactive molecules with estrogen receptors (ERs). Ethyl acetate fraction of the mother extract was proved as the AEF. AEF significantly improved various biomechanical and biochemical parameters in a dose dependent manner in the ovariectomized animals. AEF also controlled the increased body weight and decreased uterus weight following ovariectomy. Histopathology of femur revealed the restoration of typical bone structure and trabecular width in ovariectomized animals after AEF and raloxifene treatment. AEF also exhibited in vitro cytotoxicity in breast (MCF-7 and MDA-MB-231) and ovarian (SKOV-3) cancer cells. Further, genistein and daidzein exhibited a high affinity towards both estrogen receptors ( and {beta}) in docking study revealing the probable mechanism of the antiosteoporotic activity. GC/MS analysis confirmed the presence of bioactive molecules such as stigmasterol, {beta}-sitosterol, and stigmasta-3,5-dien-7-one. The observations of this study vindicate the potency of AEF from P. tuberosa in the treatment of menopausal osteoporosis and cancer.

pharmacology and toxicology↗

Isolation and molecular identification of pectinase producing Aspergillus species from different soil samples of Bhubaneswar regions

With the significant improvement of human civilization there is a spur in the urban, rural and industrial development, which has a profound effect on the surrounding natural environment. Increased utilization of natural resources is often associated with accumulation of waste materials whose management is crucial for sustainable development of life. Availability of different microorganisms in the soil facilitates the degradation of wastes through their potential enzymatic activities. Pectinase seems to be one of the important enzymes produced by a wide variety of microorganisms contained in the soil. It is mainly involved in maceration and rotting of plant extracts and debris by hydrolysis of 1,4-alpha glycosidic bonds of de-esterified pectate of plant call wall. In this paper we report molecular identification of some pectinase producing Aspergillus species selected from soil samples of five different zones of Bhubaneswar city using molecular biology and computational techniques. Among fifteen fungal isolates studied from these five zones Aspergillus parvisclerotigenus was potent for pectinase production next to Aspergillus niger in form of halozone of 0.6 mm. Its 28S rDNA sequence also had some significant identity (>90%) with different subspecies of Aspergillus. We hope that our findings will helpful in genetic manipulation for improvement of fungal strains of isolates. Again large scale use of the improved Aspergillus strains can degrade plant biomass & diverse industrial wastes which will reduce environmental pollution of capital urban like Bhubaneswar.

microbiology↗

Microscaled Proteogenomic Methods for Precision Oncology

Cancer proteogenomics integrates genomics, transcriptomics and mass spectrometry (MS)-based proteomics to gain insights into cancer biology and treatment efficacy. A proteogenomics approach was therefore developed for frozen core biopsies using tissue-sparing specimen processing with a \"microscaled\" proteomics workflow. For technical proof-of-principle, biopsies from ERBB2 positive breast cancers before and 48-72 hours after the first dose of neoadjuvant trastuzumab-based chemotherapy were analyzed. ERBB2 protein and phosphosite levels, as well as mTOR target phosphosites, were significantly more suppressed upon treatment in cases associated with pathological complete response, suggesting MS-based pharmacodynamics is achievable. Furthermore, integrated analyses indicated potential causes of treatment resistance including the absence of ERBB2 amplification (false-ERBB2 positive) and insufficient ERBB2 activity for therapeutic sensitivity despite ERBB2 amplification (pseudo-ERBB2 positive). Candidate resistance features in true-ERBB2+ cases, including androgen receptor signaling, mucin expression and an inactive immune microenvironment were observed. Thus, proteogenomic analysis of needle core biopsies is feasible and clinical utility should be investigated.

cancer biology↗

UbiFast, a rapid and deep-scale ubiquitylation profiling approach for biology and translational research

Protein ubiquitylation is involved in a plethora of cellular processes. Defects in the ubiquitin system are at the root of many acquired and hereditary diseases. While antibodies directed at ubiquitin remnants (K-{varepsilon}-GG) have improved the ability to monitor ubiquitylation using mass spectrometry, methods for highly-multiplexed measurement of ubiquitylation in tissues and primary cells using sub-milligram amounts of sample remains a challenge. Here we present a highly-sensitive, rapid and multiplexed protocol for quantifying [~]10,000 ubiquitylation sites from as little as 500 ug peptide per sample from cells or tissue in a TMT10 plex in ca. 5 hr. High-field Asymmetric Ion Mobility Spectrometry (FAIMS) is used to improve quantitative accuracy for posttranslational modification analysis. We use the approach to rediscover substrates of the E3 ligase targeting drug lenalidomide and to identify proteins modulated by ubiquitylation in models of basal and luminal human breast cancer. The sensitivity and speed of the UbiFast method makes it suitable for large-scale studies in primary tissue samples.

biochemistry↗