Biology subjects

Ravi, A. K.

Publications and source records attributed to Ravi, A. K..

3 recordsLinked to original sources

bioRxiv2026

Global protein expression profiling in stem cell factor stimulated human Acute megakaryoblastic leukemia cells identifies CFL1, GSN and CCT8 as prognostic biomarkers for Acute Myeloid Leukemia.

Abstract Background: The stem cell factor receptor or c-Kit is a type III receptor tyrosine kinase, activated by its ligand Stem cell factor (SCF). Up on activation, c-kit induces signaling pathways that regulates blood cell proliferation, survival, differentiation, and migration. Several studies reported that c-Kit/SCF signaling, contributes to the development and progression of acute myeloid leukemia (AML) in patients. However, the downstream proteins regulated by c-kit activation and their clinical significance in AML remain poorly explored. Methods: Human Acute megakaryoblastic leukemia (Mo7e) cells, were-stimulated with SCF and global protein expression were profiled using two-dimensional gel electrophoresis coupled with MALDI-TOF and LC-MS/MS. Differentially expressed proteins were functionally characterized and validated using patient data from the TCGA-LAML and matched normal data from GTEx, GEO datasets, and quantitative RT-PCR. Their diagnostic and prognostic significance was assessed using ROC, Cox regression, LASSO, Kaplan Meier survival analyses, and a prognostic nomogram model. Results: Proteomic profiling identified 14 differentially expressed proteins in SCF-stimulated Mo7e cells, which are predicted to involved in cytoskeletal organization, protein folding, metabolism, vesicular trafficking, and translational regulation. Transcriptomic analysis of the TCGA-LAML cohort revealed significant dysregulation of CFL1, CCT8, HSP90B1, MDH2, EIF5A, GSN, and TPI1. Integrated ROC, Cox regression, and LASSO analyses identified CFL1, CCT8, and GSN as the most robust prognostic biomarkers associated with poor overall survival in LAML patients. Their expression patterns were validated in independent GEO datasets and by qRT-PCR in SCF stimulated Mo7e cells. Finally, a three-gene nomogram model was developed and validated to predict the overall survival probability of AML patients at 1-, 3-, and 5-year time points. Conclusions: This study identifies CFL1, CCT8, and GSN as key downstream effectors of c-Kit signaling as prognostic biomarkers for AML. These findings provide mechanistic insights into c-Kit-driven leukemogenesis and establish a clinically relevant three-gene signature for AML risk stratification and potential therapeutic targeting.

cancer biology↗

bioRxiv2025

Enhancing the biocorrosion resistance and biocompatibility of Aluminium substrates using Graphene Oxide-PEDOT:PSS Hybrid Coating

Biofilm-associated infections on medical devices remain a major clinical challenge due to antimicrobial resistance, biofouling, and biocorrosion, compromising implant longevity and biocompatibility. Conventional biomedical devices utilizing stainless steel and titanium exhibit limited resistance to biofilm-prone physiological environments, necessitating development of next-generation implant materials. While alumina (Al2O3) is favored for its bio-inertness, it raises concerns like leaching and systemic toxicity. Aluminum alloy 1050 (AA1050) offers intrinsic corrosion resistance via a passive oxide layer under dry conditions but remains prone to microbiologically influenced corrosion (MIC) under humid conditions. In the recent years, graphene family of materials have emerged as promising surface coating for metals and alloys due to their strong barrier properties and antimicrobial efficacy. Most graphene derivatives like GO require relatively higher concentrations to achieve antimicrobial activity, however compromising biocompatibility, limiting in vivo human uses. This study addresses these caveats by exploring GO activity at lower concentrations (50-500 {micro}g/ml) on AA1050 to achieve a balance between antimicrobial efficiency and cytocompatibility. Additionally, poly(3,4-ethylenedioxythiophene):poly(styrenesulfonate) (PEDOT:PSS, 1 {micro}g/ml) was integrated with GO to form a hybrid coating on Al (Al_GO/P), to improve GO adhesion, and corrosion resistance. Biological evaluations against Escherichia coli (E. coli), Staphylococcus aureus (S. aureus), and Candida albicans (C. albicans) demonstrated superior antifouling and antimicrobial efficacy of Al_GO/P substrates compared to GO-coated Al (Al_GO) and bare Al surfaces. Corrosion rate, FESEM, ICP-MS, and cytotoxicity analyses further confirmed reduced biocorrosion, minimal ion leaching, along with enhanced biocompatibility of the hybrid coated surfaces. Al_GO/P containing GO at 100 and 250 {micro}g/ml concentration achieved the optimal balance between antimicrobial activity and biocompatibility and can be used as in vivo implant materials. Hence, this technology can be implemented towards surface modification of biomedical devices to mitigate periprosthetic infections as well as support ex vivo applications requiring durable antimicrobial performance.

microbiology↗

bioRxiv2024

Mitochondrial DNA Mutations Linking Leigh Syndrome and Carotid Atherosclerosis: A Study of Shared Genetic Pathways

Mitochondrial DNA encodes the genetic information necessary for mitochondrial function. In humans, mitochondrial DNA spans 16,569 base pairs while representing a small fraction of the genetic material in humans. Due to their higher mutation rates compared to nuclear DNA, Mitochondrial DNA mutations are emerging as promising biomarkers for assessing disease predisposition and progression. This in-silico analyzes the correlation between Mitochondrial DNA mutations and two conditions: Leigh syndrome, a severe neurodegenerative disorder, and carotid atherosclerosis, a major cardiovascular disease. We focus on five single nucleotide variants (SNVs) - m.14459G>A, m.13513G>A, m.12315G>A, m.1555A>G, and m.15059G>A - to explore their roles in both diseases. Our findings suggest that mutations m.14459G>A, m.1555A>G, and m.15059G>A contribute to the pathogenesis of both conditions. In contrast, m.12315G>A is linked to MELAS syndrome and carotid atherosclerosis. Interestingly, the m.13513G>A mutation is associated with Leigh syndrome but negatively correlated with atherosclerosis, suggesting a potential protective effect. These SNVs could serve as targets for diagnostic and therapeutic approaches, enhancing our understanding of the genetic basis of these diseases.

bioinformatics↗