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In JoVE (3)
- Bilayer लचीला गुण में निगरानी परिवर्तन के लिए एकल अणु तरीके
- कृत्रिम bilayers इलैक्ट्रोफिजियोलॉजी प्रयोगों के लिए तैयार
- छोटे अणुओं लिपिड bilayer गुण को संशोधित करने के लिए संभावित निर्धारण के लिए, Gramicidin आधारित प्रतिदीप्ति परख
Other Publications (2)
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Articles by Ruchi Kapoor in JoVE
JoVE General
Bilayer लचीला गुण में निगरानी परिवर्तन के लिए एकल अणु तरीके
1Department of Physiology and Biophysics, Weill Cornell Medical College, 2Department of Physiology and Biophysics, Weill Cornell Medical College of Cornell University
झिल्ली प्रोटीन समारोह कोशिका झिल्ली लिपिड संरचना द्वारा विनियमित है. यह वीडियो लेख जानकारी कैसे बदल झिल्ली गुण के संवाददाताओं के रूप में bilayer पैच इलेक्ट्रोड, के रूप में के रूप में कैसे उपयोग करने के लिए में अच्छी तरह से gramicidin चैनलों का उपयोग कर पैच फार्म.
JoVE General
कृत्रिम bilayers इलैक्ट्रोफिजियोलॉजी प्रयोगों के लिए तैयार
Department of Physiology and Biophysics, Weill Cornell Medical College of Cornell University
Planar लिपिड bilayers, भी कहा जाता है कृत्रिम लिपिड bilayers, आप का अध्ययन करने के लिए अनुमति आयन एक अच्छी तरह से परिभाषित वातावरण में चैनलों का आयोजन. यहाँ, हम व्यक्ति bilayer कक्ष तैयार करने के लिए आवश्यक कदम, इलेक्ट्रोड और कैसे करने के लिए परीक्षण है कि bilayer एकल चैनल माप के लिए उपयुक्त है प्रदर्शित करता है.
JoVE General
छोटे अणुओं लिपिड bilayer गुण को संशोधित करने के लिए संभावित निर्धारण के लिए, Gramicidin आधारित प्रतिदीप्ति परख
Department of Physiology and Biophysics, Weill Cornell Medical College
हम एक तेजी से प्रतिदीप्ति आधारित परख कि gramicidin चैनल गतिविधि का एक उपाय के रूप में प्रतिदीप्ति शमन की दर पर नज़र रखता है परिचय. लिपिड bilayer गुणों में परिवर्तन के रूप में bilayer फैले प्रोटीन से महसूस की निगरानी gramicidin चैनल आणविक बल transducers के रूप में उपयोग किया जाता है.
Other articles by Ruchi Kapoor on PubMed
Variant Brain-derived Neurotrophic Factor (Val66Met) Alters Adult Olfactory Bulb Neurogenesis and Spontaneous Olfactory Discrimination
Neurogenesis, the division, migration, and differentiation of new neurons, occurs throughout life. Brain derived neurotrophic factor (BDNF) has been identified as a potential signaling molecule regulating neurogenesis in the subventricular zone (SVZ), but its functional consequences in vivo have not been well defined. We report marked and unexpected deficits in survival but not proliferation of newly born cells of adult knock-in mice containing a variant form of BDNF [a valine (Val) to methionine (Met) substitution at position 66 in the prodomain of BDNF (Val66Met)], a genetic mutation shown to lead to a selective impairment in activity-dependent BDNF secretion. Utilizing knock-out mouse lines, we identified BDNF and tyrosine receptor kinase B (TrkB) as the critical molecules for the observed impairments in neurogenesis, with p75 knock-out mice showing no effect on cell proliferation or survival. We then localized the activated form of TrkB to a discrete population of cells, type A migrating neuroblasts, and demonstrate a decrease in TrkB phosphorylation in the SVZ of Val66Met mutant mice. With these findings, we identify TrkB signaling, potentially through activity dependent release of BDNF, as a critical step in the survival of migrating neuroblasts. Utilizing a behavioral task shown to be sensitive to disruptions in olfactory bulb neurogenesis, we identified specific impairments in spontaneous olfactory discrimination, but not general olfactory sensitivity or habituation to olfactory stimuli in BDNF mutant mice. Through these observations, we have identified novel links between genetic variant BDNF and adult neurogenesis in vivo, which may contribute to significant impairments in olfactory function.
Lipid Bilayer Regulation of Membrane Protein Function: Gramicidin Channels As Molecular Force Probes
Membrane protein function is regulated by the host lipid bilayer composition. This regulation may depend on specific chemical interactions between proteins and individual molecules in the bilayer, as well as on non-specific interactions between proteins and the bilayer behaving as a physical entity with collective physical properties (e.g. thickness, intrinsic monolayer curvature or elastic moduli). Studies in physico-chemical model systems have demonstrated that changes in bilayer physical properties can regulate membrane protein function by altering the energetic cost of the bilayer deformation associated with a protein conformational change. This type of regulation is well characterized, and its mechanistic elucidation is an interdisciplinary field bordering on physics, chemistry and biology. Changes in lipid composition that alter bilayer physical properties (including cholesterol, polyunsaturated fatty acids, other lipid metabolites and amphiphiles) regulate a wide range of membrane proteins in a seemingly non-specific manner. The commonality of the changes in protein function suggests an underlying physical mechanism, and recent studies show that at least some of the changes are caused by altered bilayer physical properties. This advance is because of the introduction of new tools for studying lipid bilayer regulation of protein function. The present review provides an introduction to the regulation of membrane protein function by the bilayer physical properties. We further describe the use of gramicidin channels as molecular force probes for studying this mechanism, with a unique ability to discriminate between consequences of changes in monolayer curvature and bilayer elastic moduli.
