Molecular Receptors Research Articles

Anti-Hormonal Therapy in Breast Cancer and Its Effect on the Blood-Brain Barrier.

Simple SummaryAnti-hormonal therapie regimes are well established in oncological treatments in breast cancer. In contrast there is limited knowledge of their effects on metastatic brain metastases in advanced breast cancer and their ability to cross the blood brain-barrier. In this review, we point out the usual antihormonal therapy options in the primary disease, but also in metastatic breast cancer. In addition, we explain the epidemiological facts of brain metastases, as well as the basics of the blood-brain barrier and how this is overcome by metastase. Last but not least, we deal with the known anti-hormonal therapy options and present clinical studies on their intracerebral effect, as well as the known basics of their blood-brain barrier penetration. Not all common anti-hormonal therapeutics are able to penetrate the CNS. It is therefore important for the treating oncologists to use substances that have been proven to cross the BBB, despite the limited data available. Aromataseinhibitors, especially letrozole, probably also tamoxifen, everolimus and CDK4/6 inhibitors, especially abemaciclib, appear to act intracerebrally by overcoming the blood-brain barrier. Nevertheless, further data must be obtained in basic research, but also health care research in relation to patients with brain metastases.The molecular receptor status of breast cancer has implications for prognosis and long-term metastasis. Although metastatic luminal B-like, hormone-receptor-positive, HER2−negative, breast cancer causes brain metastases less frequently than other subtypes, though tumor metastases in the brain are increasingly being detected of this patient group. Despite the many years of tried and tested use of a wide variety of anti-hormonal therapeutic agents, there is insufficient data on their intracerebral effectiveness and their ability to cross the blood-brain barrier. In this review, we therefore summarize the current state of knowledge on anti-hormonal therapy and its intracerebral impact and effects on the blood-brain barrier in breast cancer.

TCL-486 Correlation of T-Cell Receptor Constant Beta Chain 1 (TRBC1) by Flow Cytometry With Molecular T-Cell Receptor Clonality for the Investigation of T-Cell Lymphocytosis.

Establishing clonality is an important step towards diagnosing B and T-cell lymphomas. While B-cell clonality is established quickly using flow cytometry, the gold standard for T-cell clonality involves expensive and time-consuming genetic studies. The significance of T-cell clones detected by this method are often more uncertain. More recently, TRBC1 expression on T-cells as detected by flow cytometry has been shown to be a simple, rapid and robust representation of T-cell clonality. This has been implemented in our diagnostic laboratory with clonality reported when TRBC1 expression is identified in <15% or >85% of T-cells. This study examines the reporting of TRBC1 based clonality using flow cytometry and molecular clonality results in the investigation of T-cell lymphocytosis. All cases tested for T-cell clonality by the molecular laboratory at RMH between 05/04/2021 and 10/11/2021 were identified retrospectively. Molecular and immunophenotyping results were extracted from electronic patient records (EPR). We analyzed TRBC1 status and T-cell receptor (TCR) clonality by molecular rearrangements including TCR beta (TCRB) and TCR gamma (TCRG). 284 cases were identified. TRBC1 status as detected by flow cytometry was documented in 82 cases. Our laboratory reported a clonal population by TRBC1 in 27/82 cases. In all 27 cases a clonal T-cell population was also identified in both TCRB and TCRG by molecular testing. In 1 case molecular studies failed due to lack of amplification. No clonal TRBC1 population was described as per laboratory cut-offs in 55 cases. 17/55 were also reported as polyclonal by molecular studies. A weak clonal population of uncertain significance was detected in 4/55 cases. There were clonal populations detected by molecular studies in 31/55 of these cases. In 3/55 cases molecular studies failed. 100% of cases with clonal TRBC1 detected by flow cytometry demonstrate T-cell clonality on molecular testing. As per current reporting standards defined in our laboratory, small T cell clones are not reported due to the unknown clinical significance leading to a discrepancy between reports by flow and molecular laboratories. The clinical context and outcomes of these cases is being investigated to understand the clinical significance.

Poster: TCL-486 Correlation of T-Cell Receptor Constant Beta Chain 1 (TRBC1) by Flow Cytometry With Molecular T-Cell Receptor Clonality for the Investigation of T-Cell Lymphocytosis

Poster: TCL-486 Correlation of T-Cell Receptor Constant Beta Chain 1 (TRBC1) by Flow Cytometry With Molecular T-Cell Receptor Clonality for the Investigation of T-Cell Lymphocytosis

Protection and Transformation of Natural Products within Aqueous Metal‐Organic Cages

AbstractNatural products are central to the organic synthesis field and attract immense interest due to their biological activity and wide industrial use. However, many suffer from poor aqueous solubility, instability under certain conditions, or bear complex composition, limiting their investigation and derivatization. Metal–organic cages (MOCs) are promising molecular receptors to solubilize in water, preserve, or transform natural products. This contribution features examples of MOCs that encapsulate naturally occurring compounds and synthetic congeners in aqueous media, protecting them from photodegradation or hydrolysis. We highlight cases of cages used as molecular vessels to promote chemical conversion and derivatization of natural substances. This review aims to provide an overview of the possibilities of using MOCs to bring about new properties and reactivity on natural products, offering methodological insights into cage operation for enhancing their activity and the engineering of further aqueous applications involving natural compounds, synthetic derivatives, and biomolecules.

Macrocyclic ligand-embedded graphene-in-polymer nanofiber membranes for lithium ion recovery

Ensuring a stable and diverse lithium supply is becoming increasingly important for battery-related industries. Herein, we propose the concept of integrating a molecular receptor and graphene-in-polymer nanofibers to create highly durable and reusable membranes for selective lithium ion recovery. Specifically, macrocyclic chelating ligand (12C4) molecules as ion receptors were incorporated into a graphene-in-polyethersulfone (PES) nanofiber (CGPNF) membrane. The CGPNF membranes with diameters of approximately 100 nm showed an increase in diameter and surface roughness after lithium ion adsorption. Theoretical calculations indicated that the graphene nanosheets provide intermolecular interactions for the uniform dispersion and stable entrapment of the molecular receptors in the nanofibers. In addition, nitrogen sorption tests revealed that the graphene nanosheets improve the stability of the nanofibers, allowing for more effective porosity and surface area. The graphene nanosheets also increased the surface roughness and chemical inhomogeneity of the CGPNF membrane, thereby increasing its hydrophilicity. The adsorption isotherms of the CGPNF membranes were more accurately described by a pseudo second-order model, indicating that the adsorption kinetics are governed by a chemisorption process, namely, host–guest interactions. Finally, in a flow system, the CGPNF membrane showed a maximum adsorption capacity of 86.3 mg g−1 for lithium ions and retained more than 93 % of its initial adsorption capacity after 10 regeneration cycles.

Molecular imprinting synthetic receptor based sensor for determination of Parkinson's disease biomarker DJ-1

Parkinson's disease (PD) is one of the neurological disorders with severe motor and non-motor dysfunction. PARK7/DJ-1 is reported as a highly sensitive PD biomarker protein. So, the DJ-1 protein was chosen as the target protein for the fabrication of a MIP based sensor here. This work reports the fabrication and development of molecularly imprinted polypyrrole (MIPPy) on a screen printed carbon electrode (SPCE) surface for DJ-1 protein recognition.The MIPPy DJ-1 imprinted sensor was carried out by electropolymerization of pyrrole (Py) monomer on a SPCE electrode using cyclic voltammetry (CV) in order to obtain highly selective nano matrices with high molecular recognition capability.Also, the AuNP conjugated impedimetric immunosensor was fabricated for comparison with the MIPPy sensor. MIPPy / immuno sensors were characterized through cyclic voltammetry (CV), electrochemical impedance spectroscopy (EIS), and scanning electron microscopy (SEM). The analytical performance of the MIPPy-based sensor (detection 1 nM; linear range: 1 nM to 500 nM) was comparable with that of the DJ-1 immunosensor (detection limit 1 nM; linear range: 1 nM to 500 nM). These MIPPy/immuno sensors were successfully applied in the DJ-1 analysis in over-expressed and control N2A cells. Also the MIPPy based sensor gave an excellent correlation with AuNP/PPy immunosensor and Western Blot.

Molecular Characteristics, Receptor Specificity, and Pathogenicity of Avian Influenza Viruses Isolated from Wild Ducks in Russia.

Avian influenza viruses (AIV) of wild ducks are known to be able to sporadically infect domestic birds and spread along poultry. Regular surveillance of AIV in the wild is needed to prepare for potential outbreaks. During long-year monitoring, 46 strains of AIV were isolated from gulls and mallards in Moscow ponds and completely sequenced. Amino acid positions that affect the pathogenicity of influenza viruses in different hosts were tested. The binding affinity of the virus for receptors analogs typical for different hosts and the pathogenicity of viruses for mice and chickens were investigated. Moscow isolates did not contain well-known markers of pathogenicity and/or adaptation to mammals, so as a polybasic cleavage site in HA, substitutions of 226Q and 228G amino acids in the receptor-binding region of HA, and substitutions of 627E and 701D amino acids in the PB2. The PDZ-domain ligand in the NS protein of all studied viruses contains the ESEV or ESEI sequence. Although several viruses had the N66S substitution in the PB1-F2 protein, all Moscow isolates were apathogenic for both mice and chickens. This demonstrates that the phenotypic manifestation of pathogenicity factors is not absolute but depends on the genome context.

Nodule formation in Bombyx mori larvae is regulated by BmToll10-3

Nodule formation is a two-step cell-mediated immune response that is elicited by the cytokine spätzle1. Spätzle1 is activated within 30 s of invasion by microorganisms via an extracellular signaling pathway that consists of pathogen-associated molecular pattern recognition receptors, C-type lectins, and serine proteases. Here, we investigated a hemocyte molecule that is involved in eliciting the first step of nodule formation. BmToll10-3 was one of 14 Toll homologs identified in the silkworm Bombyx mori; it is an ortholog of Spodoptera exigua Toll. Previous research suggested that SeToll elicits nodule formation, but no evidence was presented to indicate whether SeToll elicited the first or second step of nodule formation. Reverse transcription-polymerase chain reaction and immunostaining confirmed that BmToll10-3 is expressed in granulocytes. To determine whether BmToll10-3 is involved in eliciting the first step of nodule formation, we tested an antiserum raised against BmToll10-3 in a nodule formation assay. The antiserum strongly inhibited the first step of nodule formation in B. mori larvae. Next, we tried to knock out BmToll10-3 using genome editing. Strains that were heterozygous for a truncated BmToll10-3 allele were generated, but no strain that was homozygous for truncated BmToll10-3 was generated. Nonetheless, several healthy homozygous larvae were identified before pupation, and we used these larvae in a nodule formation assay. The larvae that were homozygous for truncated BmToll10-3 did not form nodules. These results suggest that BmToll10-3 is involved in a cellular immunity, nodule formation.

The dendritic cell receptor Clec9A: receptor regulation and immune modulation

Dendritic cells (DC) use a variety of cell surface receptors to monitor the environment for potential dangers, including cells that have died of non-homeostatic causes (eg. infected cells), to induce appropriate immune responses. Clec9A is a DC-specific Damage-Associated Molecular Pattern receptor, that is expressed by mouse and human cross-presenting DC subsets. Clec9A recognises actin filaments exposed on dead cells, and facilitates the processing of dead cell-derived antigen (Ag) for the induction of effective immune responses. A major focus of our research is identification of the molecular mechanisms that underpin Clec9A function and the control of immune responses to dead cell-associated Ag, and on the development of Clec9A-targeting approaches for enhancing immune responses. We recently identified a novel intracellular Clec9A-binding partner, the E3 ubiquitin ligase, RNF41. We discovered RNF41 ubiquitinates Clec9A to regulate its downstream fate. Intriguingly, RNF41 ubiquitinates the extracellular domains of Clec9A, revealing a novel mechanism of receptor regulation. Furthermore, RNF41 regulates DC cross-presentation of Ag acquired from dead cells. Our research is now focussed on elucidating this novel pathway of Clec9A regulation, and the role of this pathway in regulating MHCI processing and presentation of dead cell Ag.

Extracellular vesicles derived from PPRV-infected cells enhance signaling lymphocyte activation molecular (SLAM) receptor expression and facilitate virus infection.

Peste des petits ruminants virus (PPRV) is an important pathogen that seriously influences the productivity of small ruminants worldwide. PPRV is lymphotropic in nature and SLAM was identified as the primary receptor for PPRV and other Morbilliviruses. Many viruses have been demonstrated to engage extracellular vesicles (EVs) to facilitate their replication and pathogenesis. Here, we provide evidence that PPRV infection significantly induced the secretion levels of EVs from goat PBMC, and that PPRV-H protein carried in EVs can enhance SLAM receptor expression in the recipient cells via suppressing miR-218, a negative miRNA directly targeting SLAM gene. Importantly, EVs-mediated increased SLAM expression enhances PPRV infectivity as well as the expression of various cytokines related to SLAM signaling pathway in the recipient cells. Moreover, our data reveal that PPRV associate EVs rapidly entry into the recipient cells mainly through macropinocytosis pathway and cooperated with caveolin- and clathrin-mediated endocytosis. Taken together, our findings identify a new strategy by PPRV to enhance virus infection and escape innate immunity by engaging EVs pathway.

New quinoline-thiolactone conjugates as potential antitubercular and antibacterial agents

Tuberculosis and bacterial infections are major challenges because of elevated infection rates and drug resistance. New chemical agents need to be developed to address them. Thiolactomycin and quinolines are promising lead molecules in the design of new antitubercular and antibacterial agents. Herein, we report the design and synthesis of series of new quinoline-thiolactone conjugates as potential antitubercular and antibacterial agents. Two of the conjugates, 6b and 6d, exhibited good antitubercular activity with MIC value of 8 µg/mL. Docking studies showed that the conjugates, 6b and 6d, exhibited good binding affinity towards the target protein KasA of M. tuberculosis. Two other conjugates also showed decent antibacterial activity with MIC value of 8 µg/mL. Further, the docking of conjugate 7a was better than standard drug, linezolid against three different molecular receptors.

A TrkB agonist prodrug prevents bone loss via inhibiting asparagine endopeptidase and increasing osteoprotegerin

Brain-derived neurotrophic factor (BDNF) and its tropomyosin-related kinase B receptor (TrkB) are expressed in human osteoblasts and mediate fracture healing. BDNF/TrkB signaling activates Akt that phosphorylates and inhibits asparagine endopeptidase (AEP), which regulates the differentiation fate of human bone marrow stromal cells (hBMSC) and is altered in postmenopausal osteoporosis. Here we show that R13, a small molecular TrkB receptor agonist prodrug, inhibits AEP and promotes bone formation. Though both receptor activator of nuclear factor kappa-Β ligand (RANK-L) and osteoprotegerin (OPG) induced by ovariectomy (OVX) remain comparable between WT and BDNF+/− mice, R13 treatment significantly elevates OPG in both mice without altering RANKL, blocking trabecular bone loss. Strikingly, both R13 and anti-RANK-L exhibit equivalent therapeutic efficacy. Moreover, OVX increases RANK-L and OPG in WT and AEP KO mice with RANK-L/OPG ratio lower in the latter than the former, attenuating bone turnover. 7,8-DHF, released from R13, activates TrkB and its downstream effector CREB, which is critical for OPG augmentation. Consequently, 7,8-DHF represses C/EBPβ/AEP pathway, inhibiting RANK-L-induced RAW264.7 osteoclastogenesis. Therefore, our findings support that R13 exerts its therapeutic efficacy toward osteoporosis via inhibiting AEP and escalating OPG.

Radiopharmaceutical Treatments for Cancer Therapy, Radionuclides Characteristics, Applications, and Challenges.

Advances in the field of molecular biology have had an impact on biomedical applications, which provide greater hope for both imaging and therapeutics. Work has been intensified on the development of radionuclides and their application in radiopharmaceuticals (RPS) which will certainly influence and expand therapeutic approaches in the future treatment of patients. Alpha or beta particles and Auger electrons are used for therapy purposes, and each has advantages and disadvantages. The radionuclides labeled drug delivery system will deliver the particles to the specific targeting cell. Different radioligands can be chosen to uniquely target molecular receptors or intracellular components, making them suitable for personal patient-tailored therapy in modern cancer therapy management. Advances in nanotechnology have enabled nanoparticle drug delivery systems that can allow for specific multivalent attachment of targeted molecules of antibodies, peptides, or ligands to the surface of nanoparticles for therapy and imaging purposes. This review presents fundamental radionuclide properties with particular reference to tumor biology and receptor characteristic of radiopharmaceutical targeted therapy development.

Measuring anion binding at biomembrane interfaces

The quantification of anion binding by molecular receptors within lipid bilayers remains challenging. Here we measure anion binding in lipid bilayers by creating a fluorescent macrocycle featuring a strong sulfate affinity. We find the determinants of anion binding in lipid bilayers to be different from those expected that govern anion binding in solution. Charge-dense anions H2PO4– and Cl– that prevail in dimethyl sulfoxide fail to bind to the macrocycle in lipids. In stark contrast, ClO4– and I– that hardly bind in dimethyl sulfoxide show surprisingly significant affinities for the macrocycle in lipids. We reveal a lipid bilayer anion binding principle that depends on anion polarisability and bilayer penetration depth of complexes leading to unexpected advantages of charge-diffuse anions. These insights enhance our understanding of how biological systems select anions and guide the design of functional molecular systems operating at biomembrane interfaces.

Molecular Insights of SARS-CoV-2 Infection and Molecular Treatments.

The coronavirus disease emerged in December 2019 (COVID-19) is caused by Severe Acute Respiratory Syndrome-related coronavirus 2 (SARS-CoV-2). Its rapid global spread has brought an international health emergency and urgent responses for seeking efficient prevention and therapeutic treatment. This has led to imperative needs for illustration of the molecular pathogenesis of SARS-CoV-2, identification of molecular targets or receptors, and development of antiviral drugs, antibodies, and vaccines. In this study, we investigated the current research progress in combating SARS-CoV-2 infection. Based on the published research findings, we first elucidated, at the molecular level, SARS-CoV-2 viral structures, potential viral host-cell-invasion, pathogenic mechanisms, main virus-induced immune responses, and emerging SARS-CoV-2 variants. We then focused on the main virus- and host-based potential targets and summarized and categorized effective inhibitory molecules based on drug development strategies for COVID-19 that can guide efforts for the identification of new drugs and treatment for this problematic disease. Current research and development of antibodies and vaccines were also introduced and discussed. We concluded that the main virus entry route- SARS-CoV-2 spike protein interaction with ACE2 receptors played a key role in guiding the development of therapeutic treatments against COVID-19. Four main strategies may be considered in developing molecular therapeutics, and drug repurposing is likely to be an easy, fast and low-cost approach in such a short period of time with urgent need of antiviral drugs. Additionally, the quick development of antibody and vaccine candidates has yielded promising results, but the wide-scale deployment of safe and effective COVID-19 vaccines remains paramount in solving the pandemic crisis. As new variants of the virus emerge, the efficacy of these vaccines and treatments must be closely evaluated. Finally, we discussed the possible challenges of developing molecular therapeutics for COVID-19 and suggested some potential future efforts. Despite the limited availability of literature, our attempt in this work to provide a relatively comprehensive overview of current SARS-CoV-2 studies can be helpful for quickly acquiring the key information of COVID-19 and further promoting this important research to control and diminish the pandemic.

Ultrasensitive and miniaturized ion sensors using ionically imprinted nanostructured films

The detection of ions is essential for a wide range of applications including biomedical diagnosis, and environmental monitoring among others. However, current ion sensors are based on thick sensing films (∼100 µm), requiring time-consuming preparations, and they have a limit to their sensitivity of 59 mV.Log [C]−1. Consequently, these sensors cannot be applied for high-precision applications that require high sensitivity and reduced dimensions. Furthermore, the research of anion sensors is hampered given the limited availability of molecular receptors or ionophores with acceptable performances. In this work, we overcome these limitations using a 300 nm thick sensing film based on nanoporous ion-imprinted core-shell silica/gold grafted onto a 50 nm gold film. The sensing films were highly selective towards chloride ions, compared to other anions such as nitrate, sulphate and carbonate. Moreover, this nanostructured film exhibited over 3-fold higher sensitivity (-186.4 mV.Log [C]−1) towards chloride ions compared to commercial devices. This breakthrough has led to the fabrication of the smallest and most sensitive reported anion sensor working on open circuit potentiometry, with an exceptional selectivity towards chloride ions that could be used for the measurement of chloride ions in human serum.

The neural basis of sugar preference.

When it comes to food, one tempting substance is sugar. Although sweetness is detected by the tongue, the desire to consume sugar arises from the gut. Even when sweet taste is impaired, animals can distinguish sugars from non-nutritive sweeteners guided by sensory cues arising from the gut epithelium. Here, we review the molecular receptors, cells, circuits and behavioural consequences associated with sugar sensing in the gut. Recent work demonstrates that some duodenal cells, termed neuropod cells, can detect glucose using sodium-glucose co-transporter 1 and release glutamate onto vagal afferent neurons. Based on these and other data, we propose a model in which specific populations of vagal neurons relay these sensory cues to distinct sets of neurons in the brain, including neurons in the caudal nucleus of the solitary tract, dopaminergic reward circuits in the basal ganglia and homeostatic feeding circuits in the hypothalamus, that alter current and future sugar consumption. This emerging model highlights the critical role of the gut in sensing the chemical properties of ingested nutrients to guide appetitive decisions.

Extracellular Adenosine (eAdo) - A2B Receptor Axis Inhibits in Nlrp3 Inflammasome-dependent Manner Trafficking of Hematopoietic Stem/progenitor Cells

We postulated that mobilization, homing, and engraftment of hematopoietic stem/progenitor cells (HSCPs) is facilitated by a state of sterile inflammation induced in bone marrow (BM) after administration of pro-mobilizing drugs or in response to pre-transplant myeloablative conditioning. An important role in this phenomenon plays purinergic signaling that by the release of extracellular adenosine triphosphate (eATP) activates in HSPCs and in cells in the hematopoietic microenvironment an intracellular pattern recognition receptor (PPR) known as Nlrp3 inflammasome. We reported recently that its deficiency results in defective trafficking of HSPCs. Moreover, it is known that eATP after release into extracellular space is processed by cell surface expressed ectonucleotidases CD39 and CD73 to extracellular adenosine (eAdo) that in contrast to eATP shows an anti-inflammatory effect. Based on data that the state of sterile inflammation promotes trafficking of HSPCs, and since eAdo is endowed with anti-inflammatory properties we become interested in how eAdo will affect the mobilization, homing, and engraftment of HSPCs and which of eAdo receptors are involved in these processes. As expected, eAdo impaired HSPCs trafficking and this occurred in autocrine- and paracrine-dependent manner by direct stimulation of these cells or by affecting cells in the BM microenvironment. We report herein for the first time that this defect is mediated by activation of the A2B receptor and a specific inhibitor of this receptor improves eAdo-aggravated trafficking of HSPCs. To explain this at the molecular level eAdo-A2B receptor interaction upregulates in HSPCs in NF-kB-, NRF2- and cAMP-dependent manner heme oxygenase-1 (HO-1), that is Nlrp3 inflammasome inhibitor. This corroborated with our analysis of proteomics signature in murine HSPCs exposed to eAdo that revealed that A2B inhibition promotes cell migration and proliferation. Based on this we postulate that blockage of A2B receptor may accelerate the mobilization of HSPCs as well as their hematopoietic reconstitution and this approach could be potentially considered in the future to be tested in the clinic.Graphical

Toll-like receptor 10 has a role in human macrophage response against Streptococcus pneumoniae.

Toll-like receptors (TLRs) are evolutionarily conserved pathogen-associated molecular pattern recognition receptors, and play a critical role in early response against invading pathogens. Even though TLRs have been widely studied, very little is known about the expression and function of TLR10. Till date, neither any data are available on expression of TLR10 in human lungs nor there is any information on function of TLR10 in macrophages. Streptococcus pneumoniae are Gram-positive, alpha-hemolytic, and major causative agent of pneumonia, ear infections, sinus infections, and meningitis. We examined the role of TLR10 in innate immune response to S. pneumoniae infection in U937 cell line-derived human macrophages. We found a significant increase in TLR10 mRNA and protein expression in S. pneumoniae challenged macrophages. TLR10 knockdown resulted in significant reduction of IL-1β, IL-8, IL-17, and TNF-α but not IL-10 expression in infected macrophages. TLR10 knockdown in macrophages reduced nuclear translocation of NF-κB during S. pneumoniae challenge but did not affect the phagocytosis of the bacteria. Taken together, we report the first data on TLR10's role in macrophage response against S. pneumoniae.

Metallosupramolecular Assemblies of Phthalocyanines, Subphthalocyanines and Bodipys: Photosensitizers for Visible-Light Induced Processes

Molecular self-assembly provides limitless possibilities to obtain stable and structurally well-defined supramolecules with different physicochemical properties than those of precursor building blocks. From all supramolecular interactions, strong and directional coordination-driven self-assembly allows a fine control over the rational design of two- and three-dimensional architectures with multiple potential applications. The preparation of cutting-edge metallo-supramolecular assemblies based on phthalocyanines, subphthalocyanines and BODIPYs is herein described. These ensembles have been applied for different purposes: i) as molecular receptors showing electronic interactions between the chromophore panels of the host and electroactive guests such as fullerenes and perylenediimides; ii) as hollow molecular containers able to influence a chemical reaction by providing an isolated cavity of particular size and shape, demonstrating, for example, the ability to induce unprecedented photoredox reaction with guest fullerenes, triggered by the porphyrinoid excited state; and iii) as metallosupramolecular amphiphilic systems, able to yield nanostructures via self-organization in aqueous media. Figure 1