scholarly journals Ligand−Receptor Interactions between Surfaces: The Role of Binary Polymer Spacers

Langmuir ◽  
2008 ◽  
Vol 24 (18) ◽  
pp. 10324-10333 ◽  
Author(s):  
Gabriel S. Longo ◽  
David H. Thompson ◽  
I. Szleifer
2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Linbang Wang ◽  
Tao He ◽  
Jingkun Liu ◽  
Jiaojiao Tai ◽  
Bing Wang ◽  
...  

Abstract Background Tumor-associated macrophages (TAMs) are abundant in the tumor microenvironment (TME). However, their contribution to the immunosuppressive status of the TME remains unclear. Methods We integrated single-cell sequencing and transcriptome data from different tumor types to uncover the molecular features of TAMs. In vitro experiments and prospective clinical tests confirmed the results of these analysis. Results We first detected intra- and inter-tumoral heterogeneities between TAM subpopulations and their functions, with CD86+ TAMs playing a crucial role in tumor progression. Next, we focused on the ligand-receptor interactions between TAMs and tumor cells in different TME phenotypes and discovered that aberrant expressions of six hub genes, including FLI1, are involved in this process. A TAM-tumor cell co-culture experiment proved that FLI1 was involved in tumor cell invasion, and FLI1 also showed a unique pattern in patients. Finally, TAMs were discovered to communicate with immune and stromal cells. Conclusion We determined the role of TAMs in the TME by focusing on their communication pattern with other TME components. Additionally, the screening of hub genes revealed potential therapeutic targets.


2020 ◽  
Vol 117 (37) ◽  
pp. 22690-22697 ◽  
Author(s):  
M. R. W. Scheepers ◽  
L. J. van IJzendoorn ◽  
M. W. J. Prins

Targeted drug delivery critically depends on the binding selectivity of cargo-transporting colloidal particles. Extensive theoretical work has shown that two factors are necessary to achieve high selectivity for a threshold receptor density: multivalency and weak interactions. Here, we study a model system of DNA-coated particles with multivalent and weak interactions that mimics ligand–receptor interactions between particles and cells. Using an optomagnetic cluster experiment, particle aggregation rates are measured as a function of ligand and receptor densities. The measured aggregation rates show that the binding becomes more selective for shorter DNA ligand–receptor pairs, proving that multivalent weak interactions lead to enhanced selectivity in interparticle binding. Simulations confirm the experimental findings and show the role of ligand–receptor dissociation in the selectivity of the weak multivalent binding.


2000 ◽  
pp. 115-142 ◽  
Author(s):  
Rashmin Savani ◽  
Darius Bagli ◽  
Rene Harrison ◽  
Eva Turley

2000 ◽  
Vol 74 (24) ◽  
pp. 11490-11494 ◽  
Author(s):  
Jürgen Brojatsch ◽  
John Naughton ◽  
Heather B. Adkins ◽  
John A. T. Young

ABSTRACT The identification of TVBS3, a cellular receptor for the cytopathic subgroups B and D of avian leukosis virus (ALV-B and ALV-D), as a tumor necrosis factor receptor-related death receptor with a cytoplasmic death domain, provides a compelling argument that viral Env-receptor interactions are linked to cell death (4). However, other TVB proteins have been described that appear to have similar death domains but are cellular receptors for the noncytopathic subgroup E of ALV (ALV-E): TVBT, a turkey subgroup E-specific ALV receptor, and TVBS1, a chicken receptor for subgroups B, D, and E ALV. To begin to understand the role of TVB receptors in the cytopathic effects associated with infection by specific ALV subgroups, we asked whether binding of a soluble ALV-E surface envelope protein (SU) to its receptor can lead to cell death. Here we report that ALV-E SU-receptor interactions can induce apoptosis in quail or turkey cells. We also show directly that TVBS1and TVBT are functional death receptors that can trigger cell death by apoptosis via a mechanism involving their cytoplasmic death domains and activation of the caspase pathway. These data demonstrate that ALV-B and ALV-E use functional death receptors to enter cells, and it remains to be determined why only subgroups B and D viral infections lead specifically to cell death.


2018 ◽  
Vol 62 (1) ◽  
pp. 52-58
Author(s):  
E. Káňová ◽  
I. Jiménez-Munguía ◽  
Ľ. Čomor ◽  
Z. Tkáčová ◽  
I. Širochmanová ◽  
...  

Abstract Neisseria meningitidis is a Gram-negative diplococcus responsible for bacterial meningitis and fatal sepsis. Ligand-receptor interactions are one of the main steps in the development of neuroinvasion. Porin B (PorB), neisserial outer membrane protein (ligand), binds to host receptors and triggers many cell signalling cascades allowing the meningococcus to damage the host cells or induce immune cells responses via the TLR2-dependent mechanisms. In this paper, we present a brief review of the structure and function of PorB.


2015 ◽  
Author(s):  
◽  
Kimberly J. Jasmer

Reactive oxygen species (ROS) are highly reactive, tumorigenic molecules. In response to ROS accumulation, or oxidative stress, the transcription factor Nrf2 promotes expression by binding antioxidant response elements (AREs) found in the promoter of target genes. Traditionally, Nrf2 has been considered inhibitory of cancer by promoting the expression of phase II detoxifying enzymes, drug transporters, anti-apoptotic proteins, and proteasomes, which facilitate the removal of ROS and promote cell survival. Recently, however, overexpression of Nrf2-target genes has been implicated in promoting several cancer hallmarks and facilitating cancer development. Significant focus has been given to the role of Keap1/Nrf2 as a sensor for oxidative stress. Much less attention has been paid to the role of Bach1, a transcriptional repressor that competes with Nrf2 for ARE binding. The best-characterized Bach1 target is Heme Oxygenase-1 (HMOX1). While heme oxygenase inhibits cancer by preventing ROS-induced damage, mounting evidence suggests that HMOX1 overexpression at later stages in cancer development may promote cancer progression. Heme oxygenase catalyzes the degradation of heme and has two isozymes. HMOX1 is inducible by heme and oxidative stress while HMOX2 is constitutively expressed. Stage IV metastatic melanoma has a median survival of only 6 to 10 months. Unfortunately, current therapeutic approaches provide limited benefit in overall survival, highlighting the need for the identification of novel therapeutic targets. Activating mutations in B-Raf are found in approximately 70% of malignant melanomas. Using an anchorage-independent melanosphere assay, which is indicative of the tumorigenicity of melanoma cells, we found that activation of B-Raf, but not N-Ras, is a driver of melanosphere formation. We provide evidence that derepression of Bach1 by treatment with cobalt protoporphyrin IX (CoPP) is sufficient for melanosphere formation, and that melanosphere formation induced by either CoPP treatment or B-Raf activation is dependent on heme oxygenase activity. Global transcriptome analysis revealed enrichment for genes involved in focal adhesion and extracellular matrix (ECM)-receptor interactions following either B-Raf activation or treatment with CoPP. We propose a mechanism by which heme oxygenase promotes melanosphere formation, and by extension, enhanced tumorigenicity, by modulating expression of genes involved in focal adhesion and ECM-receptor interactions. Heme oxygenase activity may provide a novel therapeutic target for the treatment of metastatic melanoma.


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