Biophysical journal最新文献

Fat4 intracellular domain controls internalization of Fat4/Dchs1 planar polarity membrane complexes.

IF 3.2 3区生物学

Biophysical journal Pub Date : 2025-02-14 DOI: 10.1016/j.bpj.2025.02.012

Yathreb Easa, Olga Loza, Roie Cohen, David Sprinzak

{"title":"Fat4 intracellular domain controls internalization of Fat4/Dchs1 planar polarity membrane complexes.","authors":"Yathreb Easa, Olga Loza, Roie Cohen, David Sprinzak","doi":"10.1016/j.bpj.2025.02.012","DOIUrl":"https://doi.org/10.1016/j.bpj.2025.02.012","url":null,"abstract":"The Fat/Dachsous (Ft/Ds) pathway is a highly conserved pathway regulating planar cell polarity (PCP) across different animal species. Proteins from the Ft and Ds family are large transmembrane protocadherins that form heterophilic complexes on the boundaries between cells. Fat4 and Dchs1, the main mammalian homologues of this pathway, have been implicated in PCP in various epithelial tissues and were shown to form extremely stable complexes at the boundaries between cells. It is unclear however, what are the dynamics controlling such stable boundary complexes, and how the formation and internalization of these complexes is regulated. Here, we use quantitative live imaging to elucidate the role of the intracellular domains (ICD) of Fat4 and Dchs1 in regulating Fat4/Dchs1 complex dynamics. We show that removing the ICD of Fat4 results in a reduction of both Trans-endocytosis (TEC) of Dchs1 into the Fat4 cells and boundary accumulation of Fat4/Dchs1 complexes, but does not affect the diffusion of the complexes at the boundary. We further show that the ICD of Fat4 controls the internalization rate of Fat4/Dchs1 complexes. Finally, we find that while actin polymerization is required for the accumulation at the boundary of Fat4/Dchs1 complexes, we do not identify correlations between Fat4/Dchs1 complexes and local actin accumulation. Overall, we suggest that the Fat4 ICD is important for the internalization and plasticity of the highly stable Fat4/Dchs1 complexes associated with PCP.","PeriodicalId":8922,"journal":{"name":"Biophysical journal","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143424930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Rab3gap1 Palmitoylation Cycling Modulates Cardiomyocyte Exocytosis and Atrial Natriuretic Peptide Release.

IF 3.2 3区生物学

Biophysical journal Pub Date : 2025-02-13 DOI: 10.1016/j.bpj.2025.02.010

Kobina Essandoh, Grace A Eramo, Arasakumar Subramani, Matthew J Brody

{"title":"Rab3gap1 Palmitoylation Cycling Modulates Cardiomyocyte Exocytosis and Atrial Natriuretic Peptide Release.","authors":"Kobina Essandoh, Grace A Eramo, Arasakumar Subramani, Matthew J Brody","doi":"10.1016/j.bpj.2025.02.010","DOIUrl":"https://doi.org/10.1016/j.bpj.2025.02.010","url":null,"abstract":"Rab3 GTPase activating protein 1 (Rab3gap1) hydrolyzes GTP on Rab3 to inactivate it and reinitiate the Rab3 cycle that regulates exocytic release of neuropeptides and hormones from neuroendocrine cells and atrial natriuretic peptide (ANP) secretion by cardiomyocytes. Cysteine palmitoylation of Rab3gap1 by the Golgi-localized S-acyltransferase zDHHC9 was recently shown to hinder ANP release by impairing Rab3gap1-mediated nucleotide cycling on Rab3a. Here we interrogated the cysteine residues of Rab3gap1 modified by palmitoylation and impacts on ANP secretion in cardiomyocytes. Although mutation of the previously identified cysteine-678 (Cys-678) site of Rab3gap1 alone was insufficient to elicit complete loss of Rab3gap1 palmitoylation in cardiomyocytes, combinatorial mutation of Cys-509, 510, 521, 522, and 678 (Rab3gap15CS) dramatically reduced Rab3gap1 palmitoylation. Notably, total cellular GAP activity in cardiomyocytes was maintained with mutation of the Rab3gap1 palmitoylation sites as the Rab3gap15CS mutant substantially reduced steady-state Rab3a-GTP levels in cardiomyocytes similar to wildtype Rab3gap1. However, while expression of wildtype Rab3gap1 induced robust secretion of ANP and greatly enhanced phenylephrine (PE)-stimulated ANP release, the Rab3gap15CS palmitoylation-deficient mutant was incapable of promoting exocytosis and ANP release by cardiomyocytes. These data suggest Rab3gap1 cysteine palmitoylation may target Rab3gap1 to Rab3a for regulated GAP-mediated inactivation at specific intracellular membrane domains to modulate the Rab3 cycle and exocytosis. Collectively, these data support a role for Rab3gap1 palmitoylation cycling in spatiotemporal control of the Rab3 cycle to regulate exocytosis and ANP secretion by cardiomyocytes.","PeriodicalId":8922,"journal":{"name":"Biophysical journal","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143424931","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Markov Models and Long-term Memory in Ion Channels: a Contradiction in Terms?

IF 3.2 3区生物学

Biophysical journal Pub Date : 2025-02-12 DOI: 10.1016/j.bpj.2025.02.006

Daniel Sigg, Vincenzo Carnevale

{"title":"Markov Models and Long-term Memory in Ion Channels: a Contradiction in Terms?","authors":"Daniel Sigg, Vincenzo Carnevale","doi":"10.1016/j.bpj.2025.02.006","DOIUrl":"https://doi.org/10.1016/j.bpj.2025.02.006","url":null,"abstract":"The opening kinetics of an ion channel are typically modeled using Markov schemes, which assume a finite number of states linked by time-independent rate constants. Although aggregate closed or open states may, under the right conditions, experience short-term (exponential) memory of previous gating events, there is experimental evidence for stretched-exponential or power-law memory decay that does not conform to Markov theory. Here, using Monte Carlo simulations of a lattice system, we investigate long-term memory in channels coupled to a heterogeneous membrane near the critical temperature. We observed that increasing the strength of the channel-lipid coupling parameter from zero to nearly 1 kT per lipid binding site leads to a progression in the autocorrelation of successive open dwell times. This evolution changes from (i) multiexponential decay to (ii) power-law decay, and finally to (iii) stretched exponential decay, mirroring changes in channel distribution from: (i) complete independence, (ii) partitioning in the interphase between lipid domains, and (iii) partitioning inside the domain favorable to the activation state of the channel. The intermediate power-law regime demonstrates characteristics of long-term memory, such as trend-reinforcing values of the Hurst exponent. Still, this regime passes a previously proposed Markovianity test utilizing conditional dwell time histograms. We conclude that low-energy state-dependent interactions between ion channels and a dynamic membrane soften the Markov assumption by maintaining a fluctuating microenvironment and storing configurational memory, supporting the existence of long memory tails without necessarily diminishing the usefulness of Markov modeling.","PeriodicalId":8922,"journal":{"name":"Biophysical journal","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143413310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Dynamical Instability is a Major Cause of Cardiac Action Potential Variability.

IF 3.2 3区生物学

Biophysical journal Pub Date : 2025-02-11 DOI: 10.1016/j.bpj.2025.02.007

Daisuke Sato, Bence Hegyi, Crystal M Ripplinger, Donald M Bers

{"title":"Dynamical Instability is a Major Cause of Cardiac Action Potential Variability.","authors":"Daisuke Sato, Bence Hegyi, Crystal M Ripplinger, Donald M Bers","doi":"10.1016/j.bpj.2025.02.007","DOIUrl":"https://doi.org/10.1016/j.bpj.2025.02.007","url":null,"abstract":"Increased beat-to-beat QT interval variability (QTV) in the electrocardiogram (ECG) is strongly associated with ventricular arrhythmias and sudden cardiac death, yet its origins remain poorly understood. While heart rate variability (HRV) decreases with deteriorating cardiac health, QTV increases, suggesting distinct underlying mechanisms. The stochastic nature of ion channel gating is a potential source of cardiac variability. However, the law of large numbers suggests that with billions of channels in the heart, this stochasticity should be minimized. In this study, we tested the hypothesis that dynamical instability amplifies stochastic ion channel fluctuations, leading to increased action potential (AP) variability. Using a mathematical model of ventricular myocytes, we investigated the relationship between AP variability and voltage instability. Our results demonstrate that stochastic gating alone cannot cause large AP variability, but dynamical instability significantly amplifies this variability. We found a positive correlation between voltage instability, indicated by the slope of the AP duration (APD) restitution curve, and APD variability. Notably, the largest variability occurred at the onset of alternans when considering every other beat. These findings provide a mechanistic explanation for increased QTV in pathological conditions and suggest that measuring QTV using every other beat may predict the onset of alternans and severity of alternans. Our study highlights the critical role of dynamical instability in cardiac electrical variability and offers new insights into the mechanisms underlying arrhythmogenesis.","PeriodicalId":8922,"journal":{"name":"Biophysical journal","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143405271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Adhesion-regulated dynamics of cells.

IF 3.2 3区生物学

Biophysical journal Pub Date : 2025-02-11 DOI: 10.1016/j.bpj.2025.01.014

Shu-Yi Sun, Xindong Chen, Bo Li, Xi-Qiao Feng

引用次数: 0

Live-Cell Imaging of Single Integrin Tensions with Minimal Background Fluorescence Noise. 以最小的背景荧光噪声进行单个整合素张力的活细胞成像。

IF 3.2 3区生物学

Biophysical journal Pub Date : 2025-02-10 DOI: 10.1016/j.bpj.2025.02.002

Vivek Pandey, Subhankar Kundu, Arghajit Pyne, Xuefeng Wang

{"title":"Live-Cell Imaging of Single Integrin Tensions with Minimal Background Fluorescence Noise.","authors":"Vivek Pandey, Subhankar Kundu, Arghajit Pyne, Xuefeng Wang","doi":"10.1016/j.bpj.2025.02.002","DOIUrl":"https://doi.org/10.1016/j.bpj.2025.02.002","url":null,"abstract":"One powerful method for studying cell mechanobiology is to monitor receptor-mediated forces at the single-molecule level in live cells. Hairpin DNA labeled with a quencher-dye pair has been used as a tension probe (TP) to image cellular forces in real time. The TP emits fluorescence when cellular forces unfold the DNA hairpin and de-quench the dye, thereby converting the force signal into fluorescence. However, when applied to monitor cellular forces at the single-molecule level, the TP often suffers from background fluorescent spots (BFSs) due to non-quenched dyes, which interfere with the molecular force imaging and analysis. In this work, we identified that the BFSs are primarily caused by missing quenchers in some TP constructs and surface-adsorbed dye-labeled DNA strands. To address these issues, we developed a double-quencher TP (dqTP) and incorporated Tween-20 treatment during surface preparation. These two simple strategies reduced the BFS level by tenfold, significantly improving the signal-to-background ratio for single molecular force imaging. We demonstrated the performance of dqTP by monitoring the temporal dynamics of integrin tensions in platelets and HeLa cells, showing that single integrin tensions remain stable for at least 100 seconds in wild-type HeLa cells. In contrast, with vinculin knocked out, a subpopulation of integrin tensions, especially at cell peripheral region, exhibited molecular force fluctuations with an average force duration shorter than 10 seconds. Overall, this work provides a convenient and practical approach to significantly reduce BFS levels on TP surfaces, offering a nearly false signal-free platform for monitoring single-molecule forces in live cells.","PeriodicalId":8922,"journal":{"name":"Biophysical journal","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143397778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Stochastic Analysis of Human Ovarian Aging and Menopause Timing.

IF 3.2 3区生物学

Biophysical journal Pub Date : 2025-02-10 DOI: 10.1016/j.bpj.2025.02.004

Anupam Mondal, Evelina Tcherniak, Anatoly B Kolomeisky

{"title":"Stochastic Analysis of Human Ovarian Aging and Menopause Timing.","authors":"Anupam Mondal, Evelina Tcherniak, Anatoly B Kolomeisky","doi":"10.1016/j.bpj.2025.02.004","DOIUrl":"https://doi.org/10.1016/j.bpj.2025.02.004","url":null,"abstract":"Menopause marks a critically important biological event that ends a woman's fertility. It is a result of ovarian aging and depletion of ovarian reserve. While many aspects of these processes are now well understood, the overall dynamic picture remains unclear. Here, we present a novel theoretical framework to analyze human ovarian aging dynamics and menopause timing. Our method is based on stochastic analysis of underlying processes stimulated by observing follicles sequentially transitioning between different stages during ovulation. This allows us to obtain a fully quantitative description of ovarian aging and menopause timing consistent with available experimental observations. Our model accurately predicts the average age of menopause across geographically diverse human populations. Theoretical analysis suggests a universal relation between the initial follicle reserve, the depletion rates, and the threshold that triggers menopause. In addition, it is found that the distributions of menopause times are quite narrow, and it is proposed that this might be a result of a precise regulation due to synchronization of transitions between different stages of follicles. Our theoretical approach not only quantitatively explains the dynamics of human ovarian aging and menopause timing, but also provides important insights into individual variability in ovarian aging. It can be used as a powerful tool for predicting menopause timing and for investigating complex processes of reproductive aging.","PeriodicalId":8922,"journal":{"name":"Biophysical journal","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143397811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Hyperactive deoxy-PIEZO1 shapes the circulatory lifecycle of irreversibly sickled cells.

IF 3.2 3区生物学

Biophysical journal Pub Date : 2025-02-08 DOI: 10.1016/j.bpj.2025.02.005

Virgilio L Lew, Simon D Rogers

{"title":"Hyperactive deoxy-PIEZO1 shapes the circulatory lifecycle of irreversibly sickled cells.","authors":"Virgilio L Lew, Simon D Rogers","doi":"10.1016/j.bpj.2025.02.005","DOIUrl":"https://doi.org/10.1016/j.bpj.2025.02.005","url":null,"abstract":"Sickle cell disease (SCD), affecting millions worldwide, is caused by the homozygous inheritance of the abnormal haemoglobin, HbS. Deoxygenation of HbS in the venous circulation permeabilizes sickle cells to calcium via PIEZO1 channels triggering a dehydration cascade driven by the outward electrochemical potassium gradient. This mechanism operates with particular intensity in a subpopulation of sickle RBCs, the irreversibly sickled cells (ISCs). The lifespan of ISCs is extremely short, about 4 to 7 days. Most of this time is spent in a profoundly dehydrated condition, the irreversibly sickled state, eliciting vaso-occlusion, which is considered the root cause of organ failure and pain crisis in SCD. There is a large experimental and clinical database on sickle cells and ISCs, but how ISCs form and evolve in the circulation remains a mystery. The present study is the first attempt to unravel the experimentally inaccessible lifecycle of ISCs in vivo applying a well-accredited model of red blood cell homeostasis and circulatory dynamics, using a vast array of validated experimental observations to tightly constrain the model parameters. The results showed that abnormally strong deoxy-PIEZO1 responses were needed for calcium to elicit a violent hyperdense collapse in ISC-destined stress reticulocytes within about a day in the circulation. The potassium-depleted ISCs remain in this maximally dehydrated but volume stable condition, the pathogenic state, sustained by vigorous pump-leak balanced sodium fluxes. Eventually, sodium pump decay initiates rapid terminal rehydration by the unbalanced net gain of NaCl and water. Analysis of the mechanisms behind this three-stage circulatory lifecycle of ISCs exposed a complex web of interactions among many components of the homeostatic fabric of RBCs. These findings point to the abnormally intense PIEZO1 response to deoxygenation in ISC-destined stress reticulocytes as a prime cause of ISC formation in vivo, a central target for future research.","PeriodicalId":8922,"journal":{"name":"Biophysical journal","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Multiple Structural States in an Intrinsically Disordered Protein, SNAP-25, Using Circular Dichroism.

IF 3.2 3区生物学

Biophysical journal Pub Date : 2025-02-08 DOI: 10.1016/j.bpj.2025.02.003

Jarom S Sumsion, Samuel W Shumway, Tanner M Blocker, Thomas D Weed, Tasha M Chambers, Ryan J Poland, Dixon J Woodbury

{"title":"Multiple Structural States in an Intrinsically Disordered Protein, SNAP-25, Using Circular Dichroism.","authors":"Jarom S Sumsion, Samuel W Shumway, Tanner M Blocker, Thomas D Weed, Tasha M Chambers, Ryan J Poland, Dixon J Woodbury","doi":"10.1016/j.bpj.2025.02.003","DOIUrl":"https://doi.org/10.1016/j.bpj.2025.02.003","url":null,"abstract":"SNAP-25, together with other SNARE proteins, drives fusion of synaptic vesicles with the nerve cell membrane leading to neurotransmitter release. It is unique in contributing two α-helices to the four-helix bundle known as the SNARE complex. Complex formation drives fusion as these proteins transform from a disordered-to-ordered (coiled-coil) state. SNAP-25 has two isoforms, -25A and -25B, but little is known of any structural differences, nor are there extensive reports of the structures of its two helical domains, SN1 and SN2. Thus, the benefit of having two distinct isoforms of SNAP-25, each with two distinct domains, is unknown. Here, we use Circular Dichroism (CD) Spectroscopy and Mass Spectrometry (MS) to further characterize the secondary structure of SNAP-25A, SNAP-25B, SN1, SN2, and a cysteine-free version of SNAP-25A. We demonstrate that these proteins undergo structural transitions, with changing fractions of α-helix, β-sheet, and random-coil. These different structures can be induced by varying the environmental conditions of ionic strength, pH, temperature, or redox state. We use triangle plots to directly display the change in ternary composition following changes in these four parameters. We report that SNAP-25A and SNAP-25B make distinctly different structural changes. We show that the secondary structure of SN1 is more variable than SN2. These data add to the ongoing literature characterizing SNAP-25 as an intrinsically disordered protein that is sensitive to environmental conditions in neuronal cells and may function as a redox sensor to modulate neurotransmitter release.","PeriodicalId":8922,"journal":{"name":"Biophysical journal","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143373602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The role of peptide conformation presented by MHC in the induction of TCR triggering.

IF 3.2 3区生物学

Biophysical journal Pub Date : 2025-02-07 DOI: 10.1016/j.bpj.2025.02.001

Andrey V Golovin, Sergey Panteleev, Alexander S Zlobin, Nadia Anikeeva, Ivan Smirnov, Alexander Gabibov, Yuri Sykulev

{"title":"The role of peptide conformation presented by MHC in the induction of TCR triggering.","authors":"Andrey V Golovin, Sergey Panteleev, Alexander S Zlobin, Nadia Anikeeva, Ivan Smirnov, Alexander Gabibov, Yuri Sykulev","doi":"10.1016/j.bpj.2025.02.001","DOIUrl":"https://doi.org/10.1016/j.bpj.2025.02.001","url":null,"abstract":"High resolution crystal structure of stimulatory peptide-MHC (pMHC) ligands bound to TCR revealed different conformation of the two peptides at positions P6 and V7 compared to the conformation of the same peptides presented by unliganded MHC. Supercomputer simulation and well-tempered metadynamics approach revealed several meta-stable non-canonical TCR-pMHC interactions that depend on the conformation of the MHC-bound peptides. The diversity of meta-stable states was significantly more represented in signaling TCR-pMHC complex. These findings suggest that TCR-pMHC recognition can be informed by a conformation of peptide presented by MHC that notably influences the orientation of TCR recognizing pMHC ligand. It appears that TCR bound to stimulatory pMHC possess a significantly higher degree of freedom to assume various metastable TCR orientations which are distinct from canonical docking. In contrast, TCR interacting with non-stimulatory pMHC ligand revealed markedly less meta-stable non-canonical interactions and disengaged from the pMHC. This suggests that productive TCR-mediated signaling may depend on non-canonical interactions between TCR and pMHC, either facilitating early recognition events or providing new contacts for catch-bond formation. Our discovery can inform future attempts to simulate the catch-bond formation mechanism in TCR-pMHC recognition, allowing the formation of new bonds mediating alternative peptide presentation.","PeriodicalId":8922,"journal":{"name":"Biophysical journal","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143373608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0