Imagerie moléculaire : vers une chimie<i>in cellulo</i>

Triller, Antoine

doi:10.1051/medsci/2011275001

Cited by 1 publication

(1 citation statement)

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“…SM approaches reveal transient interactions that lead adhesion molecules and their partners to enter and exit contacts, focal adhesions or others. Such structures can thus be created, strengthened, weakened, suppressed or simply maintained by a homeostatic equilibrium of inflows and outflows, depending on the context (Triller, 2011). Our results raise issues about adhesion strengthening mechanisms, like recruitment of intracellular scaffolds, such as the cytoskeleton, or extracellular matrix reorganization.…”

Section: Discussionmentioning

confidence: 76%

Analyzing normal and disrupted leukemic stem cell adhesion to bone marrow stromal cells by single-molecule tracking nanoscopy

Gorshkova

Cappaï

Maillot

et al. 2021

Journal of Cell Science

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Leukemic stem cells (LSCs) adhere to bone niches through adhesion molecules. These interactions, which are deeply reorganized in tumors, contribute to LSC resistance to chemotherapy and leukemia relapse. However, LSC adhesion mechanisms and potential therapeutic disruption using blocking antibodies remain largely unknown. Junctional adhesion molecule C (JAM-C, also known as JAM3) overexpression by LSCs correlates with increased leukemia severity, and thus constitutes a putative therapeutic target. Here, we took advantage of the ability of nanoscopy to detect single molecules with nanometric accuracy to characterize junctional adhesion molecule (JAM) dynamics at leuko-stromal contacts. Videonanoscopy trajectories were reconstructed using our dedicated multi-target tracing algorithm, pipelined with dual-color analyses (MTT2col). JAM-C expressed by LSCs engaged in transient interactions with JAM-B (also known as JAM2) expressed by stromal cells. JAM recruitment and colocalization at cell contacts were proportional to JAM-C level and reduced by a blocking anti-JAM-C antibody. MTT2col revealed, at single-molecule resolution, the ability of blocking antibodies to destabilize LSC binding to their niches, opening opportunities for disrupting LSC resistance mechanisms.

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Section: Discussionmentioning

confidence: 76%