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We are analyzing https://link.springer.com/article/10.1007/s00018-023-05072-4.

Title:
Mechano-regulation by clathrin pit-formation and passive cholesterol-dependent tubules during de-adhesion | Cellular and Molecular Life Sciences
Description:
Adherent cells ensure membrane homeostasis during de-adhesion by various mechanisms, including endocytosis. Although mechano-chemical feedbacks involved in this process have been studied, the step-by-step build-up and resolution of the mechanical changes by endocytosis are poorly understood. To investigate this, we studied the de-adhesion of HeLa cells using a combination of interference reflection microscopy, optical trapping and fluorescence experiments. We found that de-adhesion enhanced membrane height fluctuations of the basal membrane in the presence of an intact cortex. A reduction in the tether force was also noted at the apical side. However, membrane fluctuations reveal phases of an initial drop in effective tension followed by saturation. The area fractions of early (Rab5-labelled) and recycling (Rab4-labelled) endosomes, as well as transferrin-labelled pits close to the basal plasma membrane, also transiently increased. On blocking dynamin-dependent scission of endocytic pits, the regulation of fluctuations was not blocked, but knocking down AP2-dependent pit formation stopped the tension recovery. Interestingly, the regulation could not be suppressed by ATP or cholesterol depletion individually but was arrested by depleting both. The data strongly supports Clathrin and AP2-dependent pit-formation to be central to the reduction in fluctuations confirmed by super-resolution microscopy. Furthermore, we propose that cholesterol-dependent pits spontaneously regulate tension under ATP-depleted conditions.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Science
  • Education
  • Telecommunications

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 7,626,432 visitors per month in the current month.

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How Does Link.springer.com Make Money? {💸}

We see no obvious way the site makes money.

Many websites are intended to earn money, but some serve to share ideas or build connections. Websites exist for all kinds of purposes. This might be one of them. Link.springer.com might be making money, but it's not detectable how they're doing it.

Keywords {🔍}

cells, tension, fig, membrane, pubmed, cell, deadhesion, article, google, scholar, area, cas, fluctuations, endocytosis, rab, central, formation, control, atp, regulation, pathways, cat, data, cholesterol, pits, endocytic, endosomes, time, clathrin, excess, reduction, dynasore, sigmaaldrich, recycling, atpdepleted, regions, hela, plasma, min, imaging, phases, pit, depletion, increase, biol, early, fraction, irm, line, lot,

Topics {✒️}

1c01934/asset/images/large/nl1c01934_0005 methyl-β-cyclodextrin perturbs formation article download pdf endosome-derived clathrin-coated vesicles }_{{\text{max}}}}\frac{dq}{{ clathrin-coated pits—moving ap2 /biolphys/deserno/pdf/membrane_theory recombinant anti-rab4 antibody 10 mm methyl-ß-cyclodextrin matured calthrin-coated pit related subjects giant clathrin-coated pits de-adhesion-triggered endocytosis clathrin-coated endocytic vesicles representative colour-coded kymographs adhesive f-actin waves key energy-consuming molecules label clathrin-coated vesicles phosphatidylinositol 3-kinase-dependent pathways actin-membrane linker—ezrin results de-adhesion-mediated increase optical trapping experiments—validated probing membrane-cortex adhesion real-time deformability cytometry clathrin heavy chain clathrin heavy chain pink arrow-head points cholesterol-dependent mechanisms downstream cholesterol-dependent passive forms adding de-adhering medium lipid-raft-dependent mechanisms mechano-chemical feedbacks involved colour-coded confocal images efficient clathrin-mediated endocytosis power spectral density atp dep + chol dep = 11 atp dep + chol dep = 15 β-cyclodextrin modulates endocytic clathrin-coated pits blocking dynamin-dependent pathways cytoskeleton-dependent transient accumulation yellow arrow-head points internal surface-connected structures dynamin-dependent endocytic pathways blocking dynamin-dependent scission phosphate-buffered saline atp-dependent-pit formation de-adhesion favours curving passive cholesterol-dependent tubules cholesterol-dependent tubules reduce

Questions {❓}

  • Murphy-Ullrich JE (2001) The de-adhesive activity of matricellular proteins: is intermediate cell adhesion an adaptive state?

Schema {🗺️}

WebPage:
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         headline:Mechano-regulation by clathrin pit-formation and passive cholesterol-dependent tubules during de-adhesion
         description:Adherent cells ensure membrane homeostasis during de-adhesion by various mechanisms, including endocytosis. Although mechano-chemical feedbacks involved in this process have been studied, the step-by-step build-up and resolution of the mechanical changes by endocytosis are poorly understood. To investigate this, we studied the de-adhesion of HeLa cells using a combination of interference reflection microscopy, optical trapping and fluorescence experiments. We found that de-adhesion enhanced membrane height fluctuations of the basal membrane in the presence of an intact cortex. A reduction in the tether force was also noted at the apical side. However, membrane fluctuations reveal phases of an initial drop in effective tension followed by saturation. The area fractions of early (Rab5-labelled) and recycling (Rab4-labelled) endosomes, as well as transferrin-labelled pits close to the basal plasma membrane, also transiently increased. On blocking dynamin-dependent scission of endocytic pits, the regulation of fluctuations was not blocked, but knocking down AP2-dependent pit formation stopped the tension recovery. Interestingly, the regulation could not be suppressed by ATP or cholesterol depletion individually but was arrested by depleting both. The data strongly supports Clathrin and AP2-dependent pit-formation to be central to the reduction in fluctuations confirmed by super-resolution microscopy. Furthermore, we propose that cholesterol-dependent pits spontaneously regulate tension under ATP-depleted conditions.
         datePublished:2024-01-13T00:00:00Z
         dateModified:2024-01-13T00:00:00Z
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            Tension propagation
            Excess area regulation
            Cell Biology
            Biomedicine
            general
            Life Sciences
            Biochemistry
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      headline:Mechano-regulation by clathrin pit-formation and passive cholesterol-dependent tubules during de-adhesion
      description:Adherent cells ensure membrane homeostasis during de-adhesion by various mechanisms, including endocytosis. Although mechano-chemical feedbacks involved in this process have been studied, the step-by-step build-up and resolution of the mechanical changes by endocytosis are poorly understood. To investigate this, we studied the de-adhesion of HeLa cells using a combination of interference reflection microscopy, optical trapping and fluorescence experiments. We found that de-adhesion enhanced membrane height fluctuations of the basal membrane in the presence of an intact cortex. A reduction in the tether force was also noted at the apical side. However, membrane fluctuations reveal phases of an initial drop in effective tension followed by saturation. The area fractions of early (Rab5-labelled) and recycling (Rab4-labelled) endosomes, as well as transferrin-labelled pits close to the basal plasma membrane, also transiently increased. On blocking dynamin-dependent scission of endocytic pits, the regulation of fluctuations was not blocked, but knocking down AP2-dependent pit formation stopped the tension recovery. Interestingly, the regulation could not be suppressed by ATP or cholesterol depletion individually but was arrested by depleting both. The data strongly supports Clathrin and AP2-dependent pit-formation to be central to the reduction in fluctuations confirmed by super-resolution microscopy. Furthermore, we propose that cholesterol-dependent pits spontaneously regulate tension under ATP-depleted conditions.
      datePublished:2024-01-13T00:00:00Z
      dateModified:2024-01-13T00:00:00Z
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      pageEnd:22
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         Membrane homeostasis
         Tension propagation
         Excess area regulation
         Cell Biology
         Biomedicine
         general
         Life Sciences
         Biochemistry
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                     type:PostalAddress
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            name:Dhrubaditya Mitra
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                  address:
                     name:NORDITA, KTH Royal Institute of Technology and Stockholm University, Stockholm, Sweden
                     type:PostalAddress
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            address:
               name:Department of Physical Sciences, Indian Institute of Science Education and Research Kolkata, Mohanpur, India
               type:PostalAddress
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            name:Universität Bayreuth
            address:
               name:Experimental Physics I, Universität Bayreuth, Bayreuth, Germany
               type:PostalAddress
            type:Organization
      name:Ayan Banerjee
      affiliation:
            name:Indian Institute of Science Education and Research Kolkata
            address:
               name:Department of Physical Sciences, Indian Institute of Science Education and Research Kolkata, Mohanpur, India
               type:PostalAddress
            type:Organization
      name:Dhrubaditya Mitra
      affiliation:
            name:NORDITA, KTH Royal Institute of Technology and Stockholm University
            address:
               name:NORDITA, KTH Royal Institute of Technology and Stockholm University, Stockholm, Sweden
               type:PostalAddress
            type:Organization
      name:Bidisha Sinha
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      affiliation:
            name:Indian Institute of Science Education and Research Kolkata
            address:
               name:Department of Biological Sciences, Indian Institute of Science Education and Research Kolkata, Mohanpur, India
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Biological Sciences, Indian Institute of Science Education and Research Kolkata, Mohanpur, India
      name:Department of Biological Sciences, Indian Institute of Science Education and Research Kolkata, Mohanpur, India
      name:Mechanobiology Institute, National University of Singapore, Singapore, Singapore
      name:Department of Biological Sciences, Indian Institute of Science Education and Research Kolkata, Mohanpur, India
      name:NORDITA, KTH Royal Institute of Technology and Stockholm University, Stockholm, Sweden
      name:Department of Physical Sciences, Indian Institute of Science Education and Research Kolkata, Mohanpur, India
      name:Experimental Physics I, Universität Bayreuth, Bayreuth, Germany
      name:Department of Physical Sciences, Indian Institute of Science Education and Research Kolkata, Mohanpur, India
      name:NORDITA, KTH Royal Institute of Technology and Stockholm University, Stockholm, Sweden
      name:Department of Biological Sciences, Indian Institute of Science Education and Research Kolkata, Mohanpur, India

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Analytics and Tracking {📊}

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