Biology subjects

Kaur, J.

Publications and source records attributed to Kaur, J..

At least 55 records · Page 3Linked to original sources

bioRxiv2022

The lncRNA Sweetheart regulates compensatory cardiac hypertrophy after myocardial injury

After myocardial infarction in the adult heart the remaining, non-infarcted tissue adapts to compensate the loss of functional tissue. This adaptation requires changes in gene expression networks, which are mostly controlled by transcription regulating proteins. Long non-coding transcripts (lncRNAs) are now recognized for taking part in fine-tuning such gene programs. We identified and characterized the cardiomyocyte specific lncRNA Sweetheart RNA (Swhtr), an approximately 10 kb long transcript divergently expressed from the cardiac core transcription factor coding gene Nkx2-5. We show that Swhtr is dispensable for normal heart development and function, but becomes essential for the tissue adaptation process after myocardial infarction. Re-expressing Swhtr from an exogenous locus rescues the Swhtr null phenotype. Genes depending on Swhtr after cardiac stress are significantly occupied, and therefore most likely regulated by NKX2-5. Our results indicate a synergistic role for Swhtr and the developmentally essential transcription factor NKX2-5 in tissue adaptation after myocardial injury.

developmental biology↗

bioRxiv2022

A chromosome-scale assembly of Brassica carinata (BBCC) accession HC20 containing resistance to multiple pathogens and an early generation assessment of introgressions into B. juncea (AABB)

Brassica carinata (BBCC) commonly referred to as Ethiopian mustard is a natural allotetraploid containing the genomes of Brassica nigra (BB) and Brassica oleracea (CC). It is an oilseed crop endemic to the Northeastern regions of Africa. Although it is grown in a limited manner, B. carinata is of value as it is resistant/highly tolerant to most of the pathogens affecting cultivated Brassica species of the Us triangle that are grown worldwide as oilseed and vegetable crops. We report a chromosome-scale genome assembly of B. carinata accession HC20 using long-read Oxford Nanopore and Illumina sequencing and BioNano optical maps. The assembly has a scaffold N50 of ~39.8 Mb and covers ~1.11 Gb of the genome. We compared the available long-read genome assemblies of the six species of the Us triangle and found a highly conserved gene number and collinearity suggesting that B. juncea (AABB), B. napus (AACC), and B. carinata are strict allopolyploids. We cataloged the nucleotide-binding and leucine-rich repeat immune receptor (NLR) repertoire of B. carinata resulting in the identification of 465 NLRs. We investigated the extent and nature of early generation genomic interactions between the subgenomes of B. carinata and B. juncea in interspecific crosses between the two species. We found that C chromosome additions are well tolerated, with homoeologous exchanges occurring between the A and C genomes. Based on the genomic interactions, we propose strategies to utilize the interspecific crosses for transferring disease resistance from B. carinata to B. juncea and other Brassica species.

plant biology↗

bioRxiv2022

Surface glia predominantly contribute to the development of ALS/FTD in Drosophila model

Amyotrophic Lateral Sclerosis (ALS) is a neurodegenerative disorder characterized by motor neuron degeneration in the primary motor neurons. C9orf72 repeat expansion mutation is the most prevalent genetic causes of ALS/FTD. Due to the complexity of ALS, there has been no successful therapy for the condition. The traditional neurocentric concept of ALS derives in part from the assumption that the degradation of motor neuron (MN) cells in ALS is driven by cell-autonomous mechanisms, however, recent research has focused on the non-cell-autonomous pathogenic mechanisms such as glial, immune cells and blood-brain barriers participate in the degeneration of MNs in ALS. Drosophila melanogaster is widely used as a genetic model for ALS, giving essential mechanistic data on disease onset and development. Using newly developed genetic tools to individually mark each subtype of the adult glial system in the fruit fly, we demonstrate that surface glia are the major glial subtypes for the pathogenesis of C9orf72-mediated ALS/FTD.

pathology↗

bioRxiv2022

Glia-specific expression of neuropeptide receptor Lgr4 regulates development and adult physiology in Drosophila

Similar to the human brain, Drosophila glia may well be divided into several subtypes that each carry out specific functions. Glial GPCRs plays key roles in crosstalk between neurons and glia. Drosophila Lgr4 (dLgr4) is a human relaxin receptor homolog involved in angiogenesis, cardiovascular regulation, collagen remodeling, and wound healing. Recent study suggests that ilp7 might be the ligand for Lgr4 and regulates escape behavior of Drosophila larvae. Here we demonstrate that Drosophila Lgr4 expression in glial cells, not neurons, is necessary for early development, adult behavior, and lifespan. Reducing the Lgr4 level in glial cells, but not neurons, disrupts Drosophila development, although knocking down other LGR family members in glia has no impact. Adult-specific knockdown of Lgr4 in glia but not neurons reduce locomotion, male reproductive success, and animal longevity. The investigation of how glial expression of Lgr4 contributes to this behavioral alteration will increase our understanding of how insulin signaling via glia selectively modulates neuronal activity and behavior.

genetics↗

bioRxiv2022

Opsin-free optical neuromodulation and electrophysiology enabled by a soft monolithic infrared multifunctional neural interface

Controlling neuronal activity with high spatial resolution using multifunctional and minimally invasive neural interfaces constitutes an important step towards developments in neuroscience and novel treatments for brain diseases. While infrared neuromodulation is an emerging technology for controlling the neuronal circuitry, it lacks soft implantable monolithic interfaces capable of simultaneously delivering light and recording electrical signals from the brain while being mechanically brain-compatible. Here, we have developed a soft fibre-based device based on high-performance thermoplastics which are >100-fold softer than silica glass. The presented fibre-implant is capable of safely neuromodulating the brain activity in localized cortical domains by delivering infrared laser pulses in the 2 m spectral region while recording electrophysiological signals. Action and local field potentials were recorded in vivo in adult rats while immunohistochemical analysis of the tissue indicated limited microglia and monocytes response introduced by the fibre and the infrared pulses. We expect our devices to further enhance infrared neuromodulation as a versatile approach for fundamental research and clinically translatable therapeutic interventions.

neuroscience↗

bioRxiv2022

The X chromosome is a potential polarising signal for asymmetric cell divisions in meiotic cells of a nematode

The unequal partition of molecules and organelles during cell division results in daughter cells with different fates. Asymmetric cell divisions have been best characterised in systems in which extrinsic signals polarise the mother cell during cell division. However, the mechanisms of asymmetric cell division mediated by intrinsic signals, and the nature of these signals, are mostly unknown. Here we report an asymmetric cell division in the nematode Auanema rhodensis that may be cued by the X chromosome. In the wildtype XO male, the spermatocyte divides asymmetrically to generate X-bearing spermatids that inherit components necessary for sperm viability, and nullo-spermatids that inherits components to be discarded. We found that in XX mutant pseudomales, sperm components co-segregate with the X chromosome, supporting the hypothesis that the X chromosome is employed as a polarising signal for partitioning essential cytoplasmic components for sperm function.

developmental biology↗

bioRxiv2022

Identification of a suitable endogenous control miRNA in bone aging and senescence

ObjectiveMicroRNAs (miRNAs) are promising tools as biomarkers and therapeutic agents in various chronic diseases such as osteoporosis, cancers, type I and II diabetes, and cardiovascular diseases. Considering the rising interest in the regulatory role of miRNAs in bone metabolism, aging, and cellular senescence, accurate normalization of qPCR-based miRNA expression data using an optimal endogenous control becomes crucial. MethodsWe used a systematic approach to select candidate endogenous control miRNAs that exhibit high stability with aging from our miRNA sequence data and literature search. Validation of miRNA expression was performed using qPCR and their comprehensive stability was assessed using the RefFinder tool which is based on four statistical algorithms: GeNorm, NormFinder, BestKeeper, and comparative delta CT. The selected endogenous control was then validated for its stability in mice and human bone tissues, and in bone marrow stromal cells (BMSCs) following induction of senescence and senolytic treatment. Finally, the utility of selected endogenous control versus U6 was tested by using each as a normalizer to measure the expression of miR-34a, a miRNA known to increase with age and senescence. ResultsOur results show that Let-7f did not change across the groups with aging, senescence or senolytic treatment, and was the most stable miRNA, whereas U6 was the least stable. Moreover, using Let-7f as a normalizer resulted in significantly increased expression of miR-34a with aging and senescence and decreased expression following senolytic treatment. However, the expression pattern for miR-34a reversed for each of these conditions when U6 was used as a normalizer. ConclusionsWe show that optimal endogenous control miRNAs, such as Let-7f, are essential for accurate normalization of miRNA expression data to increase the reliability of results and prevent misinterpretation. Moreover, we present a systematic strategy that is transferrable and can easily be used to identify endogenous control miRNAs in other biological systems and conditions.

cell biology↗

bioRxiv2021

Whole genome resequencing and comparative genome analysis of three Puccinia striiformis f. sp. tritici pathotypes prevalent in India

Stripe rust disease of wheat, caused by Puccinia striiformis f. sp. tritici, (Pst) is one of the most serious diseases of wheat worldwide. In India, virulent stripe rust races have been constantly evolving in the North-Western Plains Zone leading to the failure of some of the most widely grown resistant varieties in the region. With the goal of studying the recent evolution of virulent races in this region, we conducted whole-genome sequencing of three prevalent Indian Pst pathotypes Pst46S119, Pst78S84 and Pst110S119. We assembled 58.62, 58.33 and 55.78 Mb of Pst110S119, Pst46S119 and Pst78S84 genome, respectively. Pathotypes were found to be highly heterozygous. Comparative phylogenetic analysis indicated the recent evolution of pathotypes Pst110S119 and Pst78S84 from Pst46S119. Pathogenicity-related genes classes (CAZyme, proteases, effectors, and secretome proteins) were identified and found to be under positive selection. Higher rate of gene family expansion was also observed in the three pathotypes. A strong association between the effector genes and transposable elements may be the source of the rapid evolution of these strains. Phylogenetic analysis differentiated the Indian races in this study from other known US, European, African and Asian races. Diagnostic markers developed for the identification of different Pst pathotypes will help tracking of yellow rust at farmers field and strategizing resistance gene deployment.

bioinformatics↗

bioRxiv2021

Type 1 diabetes risk genes mediate pancreatic beta cell survival in response to proinflammatory cytokines

Beta cells intrinsically contribute to the pathogenesis of type 1 diabetes (T1D), but the genes and molecular processes that mediate beta cell survival in T1D remain largely unknown. We combined high throughput functional genomics and human genetics to identify T1D risk loci regulating genes affecting beta cell survival in response to the proinflammatory cytokines IL-1{beta}, IFN{gamma}, and TNF. We mapped 38,931 cytokine-responsive candidate cis-regulatory elements (cCREs) active in beta cells using ATAC-seq and single nuclear ATAC-seq (snATAC-seq), and linked cytokine-responsive beta cell cCREs to putative target genes using single cell co-accessibility and HiChIP. We performed a genome-wide pooled CRISPR loss-of-function screen in EndoC-{beta}H1 cells, which identified 867 genes affecting cytokine-induced beta cell loss. Genes that promoted beta cell survival and had up-regulated expression in cytokine exposure were specifically enriched at T1D loci, and these genes were preferentially involved in inhibiting inflammatory response, ubiquitin-mediated proteolysis, mitophagy and autophagy. We identified 2,229 variants in cytokine-responsive beta cell cCREs altering transcription factor (TF) binding using high-throughput SNP-SELEX, and variants altering binding of TF families regulating stress, inflammation and apoptosis were broadly enriched for T1D association. Finally, through integration with genetic fine mapping, we annotated T1D loci regulating beta cell survival in cytokine exposure. At the 16p13 locus, a T1D variant affected TF binding in a cytokine-induced beta cell cCRE that physically interacted with the SOCS1 promoter, and increased SOCS1 activity promoted beta cell survival in cytokine exposure. Together our findings reveal processes and genes acting in beta cells during cytokine exposure that intrinsically modulate risk of T1D.

genomics↗

bioRxiv2021

Mucin-mimetic action of capsaicin improves high fat diet-induced gut barrier dysfunction in mice colon

The gut barrier - including tight junction proteins and mucus layers, is the first line of defense against physical, chemical, or pathogenic incursions. This barrier is compromised in various health disorders. Capsaicin, a dietary agonist of Transient receptor potential vanilloid 1 (TRPV1) channel, is reported to alleviate the complications of obesity. While its mode of action is well established to enhance energy expenditure, metabolism and prevent dysbiosis, the more local effects on the host gut - particularly the gut barrier and mucus system remain elusive. We employed a diet-induced obesity model to investigate the effect of capsaicin on the gut barrier and mucus production and to understand the involvement of mucus, bacteria, and TRPV1 in these phenomena. Mucin feeding reflected most of the effects produced by capsaicin, indicating that mucus modulation by capsaicin plays a crucial role in its anti-obesity effects. Capsaicin, bacteria and the host mucus system seem to act in a cyclic cascade involving TRPV1, which can be activated by capsaicin and various bacteria. These findings provide new insight into the role of TRPV1 in maintaining a healthy gut environment. HIGHLIGHTSO_LIExogenous mucin feeding produced anti-obesity effects similar to capsaicin in mice. C_LIO_LIMucin and capsaicin improved TJP expression, intestinal permeability and gut microbial diversity. C_LIO_LICapsaicin modulated bacterial diversity in vitro, independently of the host. C_LIO_LIProbiotic bacteria and butyrate activated TRPV1 in transfected HEK cells. C_LIO_LIAnti-obesity action of capsaicin is not exclusive to TRPV1 agonism. C_LIO_LICapsaicins action as colonic mucus secretagogue - plays a crucial part in its anti-obesity benefits. C_LI

pharmacology and toxicology↗

bioRxiv2021

Functional alterations in cortical processing of speech in glioma-infiltrated cortex

Recent developments in the biology of malignant gliomas have demonstrated that glioma cells interact with neurons through both paracrine signaling and electrochemical synapses. Glioma-neuron interactions consequently modulate the excitability of local neuronal circuits, and it is unclear the extent to which glioma-infiltrated cortex can meaningfully participate in neural computations. For example, gliomas may result in a local disorganization of activity that impedes the transient synchronization of neural oscillations. Alternatively, glioma-infiltrated cortex may retain the ability to engage in synchronized activity, in a manner similar to normal-appearing cortex, but exhibit other altered spatiotemporal patterns of activity with subsequent impact on cognitive processing. Here, we use subdural electrocorticography to sample both normal-appearing and glioma-infiltrated cortex during speech. We find that glioma-infiltrated cortex engages in synchronous activity during task performance in a manner similar to normal-appearing cortex, but recruits a diffuse spatial network. On a temporal scale, we show that glioma-infiltrated cortex has lower capacity for information encoding when performing nuanced tasks such as speech production of monosyllabic versus polysyllabic words. As a result, temporal decoding strategies for distinguishing monosyllabic from polysyllabic words were feasible for signals arising from normal-appearing cortex, but not from glioma-infiltrated cortex. These findings inform our understanding of cognitive processing in chronic disease states and have implications for neuromodulation and prosthetics in patients with malignant gliomas. Significance StatementAs gliomas proliferate, they infiltrate healthy brain tissue. Often, patients with such tumors in the language areas of the brain develop aphasia. Understanding how gliomas interact with normal neural circuits is critical for developing neuroprostheses that restore speech. Recent evidence demonstrates that glioma cells interact synaptically with neurons, and thus can modulate neural circuits. However, it is unclear the extent to which glioma-infiltrated cortex participates in cognitive processing. Using electrocorticography to record both glioma-infiltrated and normal-appearing cortex during speech, we found that glioma-infiltrated cortex is capable of coordinated neural responses, but has reduced capacity for information encoding. Instead, glioma-infiltrated cortex recruits a broader network of cortical regions during speech, which may represent a compensatory mechanism with implications for future neuroprostheses.

neuroscience↗

bioRxiv2021

IRC3 regulates mitochondrial translation in response to metabolic cues in Saccharomyces cerevisiae

Mitochondrial oxidative phosphorylation (OXPHOS) enzymes are made up of dual genetic origin. Mechanism regulating expression of nuclear encoded OXPHOS subunits in response to metabolic cues (glucose vs. glycerol), is significantly understood while regulation of mitochondrially encoded OXPHOS subunits is poorly defined. Here, we show that IRC3 a DEAD/H box helicase, previously implicated in mitochondrial DNA maintenance, is central to integrating metabolic cues with mitochondrial translation. Irc3 associates with mitochondrial small ribosomal subunit in cells consistent with its role in regulating translation elongation based on Arg8m reporter system. Glucose grown{Delta} irc3{rho}+ and irc3 temperature sensitive cells at 37C have reduced translation rates from majority of mRNAs. In contrast, when galactose was the carbon source, reduction in mitochondrial translation was observed predominantly from Cox1 mRNA in{Delta} irc3{rho}+ but no defect was observed in irc3 temperature sensitive cells, at 37C. In support, of a model whereby IRC3 responds to metabolic cues, suppressors of {Delta}irc3 isolated for restoration of growth on glycerol media restore mitochondrial translation differentially in presence of glucose vs. glycerol.

cell biology↗

bioRxiv2020

Mapping genetic effects on cell type-specific chromatin accessibility and annotating complex trait variants using single nucleus ATAC-seq

Gene regulation is highly cell type-specific and understanding the function of non-coding genetic variants associated with complex traits requires molecular phenotyping at cell type resolution. In this study we performed single nucleus ATAC-seq (snATAC-seq) and genotyping in peripheral blood mononuclear cells from 10 individuals. Clustering chromatin accessibility profiles of 66,843 total nuclei identified 14 immune cell types and sub-types. We mapped chromatin accessibility QTLs (caQTLs) in each immune cell type and sub-type which identified 6,248 total caQTLs, including those obscured from assays of bulk tissue such as with divergent effects on different cell types. For 3,379 caQTLs we further annotated putative target genes of variant activity using single cell co-accessibility, and caQTL variants were significantly correlated with the accessibility level of linked gene promoters. We fine-mapped loci associated with 16 complex immune traits and identified immune cell caQTLs at 517 candidate causal variants, including those with cell type-specific effects. At the 6q15 locus associated with type 1 diabetes, in line with previous reports, variant rs72928038 was a naive CD4+ T cell caQTL linked to BACH2 and we validated the allelic effects of this variant on regulatory activity in Jurkat T cells. These results highlight the utility of snATAC-seq for mapping genetic effects on accessible chromatin in specific cell types and provide a resource for annotating complex immune trait loci.

genomics↗

bioRxiv2020

Megakaryopoiesis in Dengue virus infected K562 cell promotes viral replication which inhibits endomitosis and accumulation of ROS associated with differentiation

In the human host blood Monocytes and bone marrow Megakaryocytes are implicated as major sites supporting high replication. The human K562 cell line supports DENV replication and represent Megakaryocyte-Erythrocyte progenitors (MEP), replicating features of in vivo Megakaryopoiesis upon stimulation with Phorbol esters. In this article, we report results that indicate the mutual influence of Megakaryopoiesis and DENV replication on each other, through comparison of PMA-induced differentiation of either mock-infected or DENV-infected K562 cells. We present data showing PMA-induced differentiation to drastically increase DENV replication and a concomitant augmented secretion of infectious virus. Although the mechanism is not clear yet, we show that it is not through an increased uptake of virus by differentiated cells. On the other hand, DENV replication in cells undergoing PMA-induced differentiation, interferes with major differentiation markers of Megakaryopoiesis including activation of ERK1/2 MAP Kinase, endomitosis and surface expression of platelet-specific proteins without any drastic effect on cell death. Among signaling intermediaries of the JAK-STAT pathway, we observed infection associated degradation of SOC3 protein similar to earlier observations with STAT2. DENV infection leads to accumulation of Reactive-oxygen species (ROS) in different cells including K562. PMA-induced differentiation of uninfected K562 cells also leads to intracellular ROS accumulation. Interestingly, we observed ROS accumulation to be suppressed by concomitant DENV replication in K562 cells undergoing PMA-induced differentiation. This is the first report of a model system where DENV replication suppresses intracellular ROS accumulation. The implications of these results for Megakaryopoiesis and viral replication would be discussed.Competing Interest StatementThe authors have declared no competing interest.View Full Text

microbiology↗

bioRxiv2019

Gene expression pattern of vacuolar-iron transporter-like (VTL) genes in hexaploid wheat during metal stress

Iron is one of the important micronutrients that is not just essential for the human body, but also required for crop productivity and yield-related traits. To address the Fe homeostasis in crop plants, multiple transporters belonging to the category of Major facilitator superfamily are being explored. In this direction, Vacuolar iron transporters (VIT) are being reported and have been characterized functionally as an important candidate to address biofortification in cereal crops. In the present study, the identification and characterization of new members of Vacuolar iron transporters-like proteins (VTL) was performed. Phylogenetic analyses demonstrated distinct clustering of all the VTL genes from the previously known VIT genes. Our analysis identifies multiple VTL genes from hexaploid wheat with the highest number of this gene family localized on chromosome 2. Quantitative expression analysis suggests that most of the VTL genes are induced only during the Fe surplus condition, thereby reinforcing their role metal homeostasis. Interestingly, most of the wheat VTL genes were significantly up-regulated in a tissue-specific manner under Zn, Mn and Cu deficiency conditions. Although, no significant changes in expression of wheat VTL genes were observed in roots under heavy metals, but TaVTL2, TaVTL3 and TaVTL5 were upregulated in the presence of cobalt stress. Overall, this work deals with the characterization of wheat VTL genes that could provide an important genetic resource for addressing metal homeostasis in bread wheat.

plant biology↗

bioRxiv2019

CpG-creating Mutations are Costly in Many Human Viruses

Mutations can occur throughout the virus genome and may be beneficial or deleterious. We are interested in mutations that yield a C next to a G, producing CpG sites. CpG sites are rare in eukaryotic and viral genomes. For the eukaryotes, it is thought that CpG sites are rare because they are prone to mutation when methylated. In viruses, we know less about why CpG sites are rare. A previous study in HIV suggested that CpG-creating transition mutations are more costly that similar non-CpG-creating mutations. To determine if this is the case in other viruses, we analyzed the allele frequencies of CpG-creating and non-CpG-creating mutations across various strains, subtypes, and genes of viruses using existing data obtained from Genbank, HIV Databases, and Virus Pathogen Resource. Our results suggest that CpG sites are costly for most viruses. By understanding the cost of CpG sites, we can obtain further insights into the evolution and adaptation of viruses.

evolutionary biology↗

bioRxiv2019

Comparative genomics of Alternaria species provides insights into the pathogenic lifestyle of Alternaria brassicae - a pathogen of the Brassicaceae family

Alternaria brassicae, a necrotrophic pathogen, causes Alternaria Leaf Spot, one of the economically important diseases of Brassica crops. Many other Alternaria spp. such as A. brassicicola and A. alternata are known to cause secondary infections in the A. brassicae-infected Brassicas. The genome architecture, pathogenicity factors, and determinants of host-specificity of A. brassicae are unknown. In this study, we annotated and characterised the recently announced genome assembly of A. brassicae and compared it with other Alternaria spp. to gain insights into its pathogenic lifestyle. Additionally, we sequenced the genomes of two A. alternata isolates that were co-infecting B. juncea. Genome alignments within the Alternaria spp. revealed high levels of synteny between most chromosomes with some intrachromosomal rearrangements. We show for the first time that the genome of A. brassicae, a large-spored Alternaria species, contains a dispensable chromosome. We identified 460 A. brassicae-specific genes, which included many secreted proteins and effectors. Furthermore, we have identified the gene clusters responsible for the production of Destruxin-B, a known pathogenicity factor of A. brassicae. The study provides a perspective into the unique and shared repertoire of genes within the Alternaria genus and identifies genes that could be contributing to the pathogenic lifestyle of A. brassicae.

genomics↗

bioRxiv2019

CX3CL1 binding protein-2 (CBP2) of Plasmodium falciparum binds nucleic acids

Several exported Plasmodium falciparum(Pf) proteins contribute to malaria biology through their involvement in cytoadherence, immune evasion and host cell remodelling. Many of these exported proteins and other host molecules are present in iRBC (infected red blood cell) generated extracellular vesicles (EVs), which are responsible for host cell modification and parasite development. CX3CL1 binding proteins (CBPs) present on the surface of iRBC have been reported to contribute to cytoadhesion by binding with the chemokine CX3CL1 via their extracellular domains. Here, we have characterized the cytoplasmic domain of CBP2to understand its function in parasite biology using biochemical and biophysical methods. Recombinant cytoplasmic CBP2 (rcCBP2) binds nucleic acids showing interaction with DNA/RNA. rcCBP2 shows dimer formation under non-reducing conditions highlighting the role of disulphide bonds in oligomerization while ATP binding leads to structural changes in the protein. In vitro interaction studies depict its binding with a Maurers cleft resident protein PfSBP1, which is influenced by ATP binding of rcCBP2. Our results suggest CBP2 as a two-transmembrane (2TM) receptor responsible for targeting EVs and delivering cargo to host endothelial cells. We propose CBP2 as an important molecule having roles in cytoadherence and immune modulation through its extracellular and cytoplasmic domains respectively.

molecular biology↗