Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Neuroplasticity01:01

Neuroplasticity

Neuroplasticity reflects the brain's remarkable capacity to adapt and evolve, responding dynamically to learning, experiences, or injury by reorganizing its neural circuitry. This reorganization involves creating new neural connections and refining old ones through a series of biological processes that contribute to the brain's lifelong development and adaptability.
Long-term Potentiation01:35

Long-term Potentiation

Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
Long-term Potentiation01:25

Long-term Potentiation

Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
Hebbian LTP
LTP can occur when presynaptic neurons...
Plasticity00:58

Plasticity

Plasticity is the property where an object loses its elasticity and undergoes irreversible deformation, even after the deformation forces are eliminated. If a material deforms irreversibly without increasing stress or load, then this is called ideal plasticity. For example, when a force is applied to an aluminum rod, it changes its shape, but it does not return to its original shape once the force is removed. Plastic deformation or ductility is thus a permanent deformation or change in the...
Amyloid Fibrils03:03

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining, normally used to...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

[Influence of acid stimulation on expression of acid-sensing ion channel 1a and 3 in type I cells of rat carotid body.].

Sheng li xue bao : [Acta physiologica Sinica]·2009
Same author

Identification of a novel estrogen receptor beta1 binding partner, inhibitor of differentiation-1, and role of ERbeta1 in human breast cancer cells.

Cancer letters·2009
Same author

Luttinger liquid to Al'tshuler-Aronov transition in disordered, many-channel carbon nanotubes.

ACS nano·2009
Same author

Pathological changes in multiple organs of rats with severe acute pancreatitis treated by baicalin and octreotide.

Hepatobiliary & pancreatic diseases international : HBPD INT·2009
Same author

Cellular and humoral immune responses in the early stages of diabetic nephropathy in NOD mice.

Journal of autoimmunity·2009
Same author

Tailoring optical transmission via the arrangement of compound subwavelength hole arrays.

Optics express·2009

Related Experiment Video

Updated: May 8, 2026

Implantation of a Cranial Window for Repeated In Vivo Imaging in Awake Mice
06:33

Implantation of a Cranial Window for Repeated In Vivo Imaging in Awake Mice

Published on: June 22, 2021

Recent advances in TMEM16F: structural plasticity, functional versatility, and implications for human diseases.

Li Chen1, Zhigang Qian2

  • 1Material Supply Center, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei, China.

Cell Communication and Signaling : CCS
|May 7, 2026
PubMed
Summary

This review details the calcium-activated membrane protein TMEM16F, a phospholipid scramblase and ion channel. It explores TMEM16F

Keywords:
Blood coagulationCell fusionInflammationIon channelNeurodegenerative diseasesPhospholipid scramblaseStructural mechanismsTMEM16FTumor immunity

More Related Videos

Microtransplantation of Synaptic Membranes to Reactivate Human Synaptic Receptors for Functional Studies
10:08

Microtransplantation of Synaptic Membranes to Reactivate Human Synaptic Receptors for Functional Studies

Published on: July 20, 2022

Related Experiment Videos

Last Updated: May 8, 2026

Implantation of a Cranial Window for Repeated In Vivo Imaging in Awake Mice
06:33

Implantation of a Cranial Window for Repeated In Vivo Imaging in Awake Mice

Published on: June 22, 2021

Microtransplantation of Synaptic Membranes to Reactivate Human Synaptic Receptors for Functional Studies
10:08

Microtransplantation of Synaptic Membranes to Reactivate Human Synaptic Receptors for Functional Studies

Published on: July 20, 2022

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • TMEM16F is a calcium-activated membrane protein with dual functions as an ion channel and phospholipid scramblase.
  • It plays a critical role in linking intracellular calcium signaling to plasma membrane lipid asymmetry.
  • Recent advances have elucidated TMEM16F's structure, conformational heterogeneity, and allosteric regulation by Ca²⁺, pH, and membrane environment.

Purpose of the Study:

  • To provide a comprehensive overview of TMEM16F biology, integrating recent structural, cellular, and pathological findings.
  • To highlight the mechanisms underlying TMEM16F's dual functions.
  • To summarize emerging evidence for TMEM16F's roles in physiological processes and disease pathogenesis.

Main Methods:

  • Literature review integrating structural biology, cell biology, and disease pathology studies.
  • Analysis of cell- and tissue-specific data on TMEM16F function.
  • Synthesis of information on TMEM16F regulation and its involvement in physiological and pathological conditions.

Main Results:

  • TMEM16F exhibits significant conformational heterogeneity and is allosterically regulated.
  • Membrane remodeling by TMEM16F is crucial for blood coagulation, cell fusion, cell death, immune responses, and neurodevelopment.
  • Dysregulation of TMEM16F is implicated in bleeding disorders, thromboinflammation, neurodegeneration, infections, and cancer.

Conclusions:

  • TMEM16F's dual functions are coordinated through complex regulatory mechanisms involving calcium, pH, and membrane context.
  • TMEM16F-mediated membrane dynamics are essential for numerous physiological processes.
  • Aberrant TMEM16F activity contributes to a wide range of human diseases, presenting potential therapeutic targets.