Calpain Inhibitor III
Calpain Inhibitor III structure
|
Common Name | Calpain Inhibitor III | ||
|---|---|---|---|---|
| CAS Number | 88191-84-8 | Molecular Weight | 382.45 | |
| Density | 1.2±0.1 g/cm3 | Boiling Point | 450.4±45.0 °C at 760 mmHg | |
| Molecular Formula | C22H26N2O4 | Melting Point | N/A | |
| MSDS | USA | Flash Point | 226.2±28.7 °C | |
|
Impaired Focal Adhesion Kinase-Grb2 Interaction during Elevated Activity in Hippocampal Neurons.
Int. J. Mol. Sci. 16 , 15659-69, (2015) Excitatory/inhibitory imbalances are implicated in many neurological disorders. Previously, we showed that chronically elevated network activity induces vulnerability in neurons due to loss of signal transducer and activator of transcription 3 (STAT3) signali... |
|
|
A recoverable state of axon injury persists for hours after spinal cord contusion in vivo.
Nat. Commun. 5 , 5683, (2014) Therapeutic strategies for spinal cord injury (SCI) commonly focus on regenerating disconnected axons. An alternative approach would be to maintain continuity of damaged axons, especially after contusion. The viability of such neuropreservative strategies dep... |
|
|
Different patterns of electrical activity lead to long-term potentiation by activating different intracellular pathways.
J. Neurosci. 35(2) , 621-33, (2015) Deciphering and storing information coded in different firing patterns are important properties of neuronal networks, as they allow organisms to respond and adapt to external and internal events. Here we report that hippocampal CA1 pyramidal neurons respond t... |
|
|
A re-assessment of long distance growth and connectivity of neural stem cells after severe spinal cord injury.
Exp. Neurol. 257 , 186-204, (2014) As part of the NIH "Facilities of Research Excellence-Spinal Cord Injury" project to support independent replication, we repeated key parts of a study reporting robust engraftment of neural stem cells (NSCs) treated with growth factors after complete spinal c... |
|
|
RVG-mediated calpain2 gene silencing in the brain impairs learning and memory.
Neuromolecular Med. 15(1) , 74-81, (2013) In the central nervous system, two calpain isoforms are highly expressed: calpain1 and calpain2. Here, we show for the first time that activation of the calpain isoform, calpain2, is a necessary event in hippocampal synaptic plasticity and in learning and mem... |
|
|
Filamin A interacts with the coactivator MKL1 to promote the activity of the transcription factor SRF and cell migration.
Sci. Signal. 8 , ra112, (2015) Megakaryoblastic leukemia 1 (MKL1) is a coactivator of serum response factor (SRF) that promotes the expression of genes associated with cell proliferation, motility, adhesion, and differentiation-processes that also involve dynamic cytoskeletal changes in th... |
|
|
A 10-minute prototype assay for tissue degradation monitoring in clinical specimens.
Exp. Mol. Pathol. 99 , 86-94, (2015) We recently identified alpha II spectrin as a Tissue Degradation Indicator (TDI) and demonstrated that intrinsic spectrin-breakdown levels reliably reveal tissue degradation status in biospecimens. With the present study, we introduce an in vitro biological a... |
|
|
Activity-dependent cleavage of the K-Cl cotransporter KCC2 mediated by calcium-activated protease calpain.
J. Neurosci. 32 , 11356-11364, (2012) The K-Cl cotransporter KCC2 plays a crucial role in neuronal chloride regulation. In mature central neurons, KCC2 is responsible for the low intracellular Cl(-) concentration ([Cl(-)](i)) that forms the basis for hyperpolarizing GABA(A) receptor-mediated resp... |
|
|
8-Oxoguanine causes neurodegeneration during MUTYH-mediated DNA base excision repair.
J. Clin. Invest. 122(12) , 4344-61, (2012) 8-Oxoguanine (8-oxoG), a common DNA lesion caused by reactive oxygen species, is associated with carcinogenesis and neurodegeneration. Although the mechanism by which 8-oxoG causes carcinogenesis is well understood, the mechanism by which it causes neurodegen... |
|
|
Characterization of ectopic colonies that form in widespread areas of the nervous system with neural stem cell transplants into the site of a severe spinal cord injury.
J. Neurosci. 34(42) , 14013-21, (2014) We reported previously the formation of ectopic colonies in widespread areas of the nervous system after transplantation of fetal neural stem cells (NSCs) into spinal cord transection sites. Here, we characterize the incidence, distribution, and cellular comp... |