calmodulin/atrophy

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Involvement of Calcium and Calmodulin in Membrane Deterioration during Senescence of Pea Foliage.

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The prospect that Ca(2+) promotes senescence by activating calmodulin has been examined using cut pea (Pisum sativum co Alaska) foliage as a model system. Senescence was induced by severing 17-day-old plants from their roots and maintaining them in aqueous test solutions in the dark for an

Differential modification of phosducin protein in degenerating rd1 retina is associated with constitutively active Ca2+/calmodulin kinase II in rod outer segments.

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Retinitis pigmentosa comprises a heterogeneous group of incurable progressive blinding diseases with unknown pathogenic mechanisms. The retinal degeneration 1 (rd1) mouse is a retinitis pigmentosa model that carries a mutation in a rod photoreceptor-specific phosphodiesterase gene, leading to rapid

Three different calmodulin-encoding cDNAs isolated by a modified 5'-RACE using degenerate oligodeoxyribonucleotides.

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In order to obtain the 5' ends of the three mouse calmodulin (CaM) cDNAs, we modified the standard 5' RACE (rapid amplification of cDNA ends) method to use degenerate synthetic oligodeoxyribonucleotides to prime cDNA synthesis of all three CaM mRNAs. In this modified method, the degenerate primers

Exclusion of the beta-subunit of type II calmodulin kinase for the wobbler spinal muscular atrophy gene.

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The wobbler mouse (wr) is an attractive model for studying motor neuron disease but the genetic defect is unknown. The beta-subunit of calmodulin kinase II (beta-CaMK II) is a good candidate for the wr mutation because of its chromosomal localization and tissue distribution. In this report, we found

Calmodulin inhibitors induce wallerian degeneration of mammalian peripheral nerves.

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Calmodulin-binding peptide PEP-19 modulates activation of calmodulin kinase II In situ.

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PEP-19 is a 6 kDa polypeptide that is highly expressed in select populations of neurons that sometimes demonstrate resistance to degeneration. These include the granule cells of the hippocampus and the Purkinje cells of the cerebellum. Its only identified activity to date is that of binding

Ca2+/calmodulin-dependent protein kinase II and Dimethyl Sulfoxide affect the sealing frequencies of transected hippocampal neurons.

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Traumatic injury often results in axonal severance, initiating obligatory Wallerian degeneration of distal segments, whereas proximal segments often survive. Calcium ion (Ca2+ ) influx at severed proximal axonal ends activates pathways that can induce apoptosis. However, this same Ca2+ -influx also

Proteomic profiling of medial degeneration in human ascending aorta.

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OBJECTIVE The objective of this study was the construction of a reference map for aortic medial degeneration by a proteomic approach. METHODS A proteomic profiling of the media of human ascending aorta was performed by two-dimensional electrophoresis and MALDI-TOF mass spectrometry. RESULTS A

cDNA cloning and sequencing of Ca2+/calmodulin-dependent protein kinase IIalpha subunit and its mRNA expression in diisopropyl phosphorofluoridate (DFP)-treated hen central nervous system.

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Diisopropyl phosphorofluoridate (DFP) produces delayed neurotoxicity, known as organophosphorus ester-induced delayed neurotoxicity (OPIDN), in hen, human, and other sensitive species. A single dose of DFP (1.7 mg/kg, se.) produces first mild ataxia followed by paralysis in 7-14 days in hens. DFP

Neuronal NF-κB ablation does not influence neuro-axonal degeneration in experimental autoimmune demyelination.

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Neuro-axonal damage is a major hallmark of multiple sclerosis (MS). To date, not much is known on the underlying mechanisms of neuronal degeneration. In disease model myelin oligodendrocyte glycoprotein induced experimental autoimmune encephalomyelitis (MOG-EAE), there is a significant loss of alpha

Severe intellectual disability, absence of language, epilepsy, microcephaly and progressive cerebellar atrophy related to the recurrent de novo variant p.(P139L) of the CAMK2B gene: A case report and brief review

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The CAMK2B gene encodes the β-subunit of calcium/calmodulin-dependent protein kinase II (CAMK2), an enzyme that has crucial roles in synaptic plasticity, especially in hippocampal and cerebellar neurons. Heterozygous variants in CAMK2B cause a rare neurodevelopmental disorder, with 40% of the

[Two autopsy cases of sudden death from dilated cardiomyopathy: calmodulin staining as an index of myocardial injury].

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Thirty-four years old man and fourty-one years old man were suddenly died after exercise and drinking, respectively. Autopsy and microscopic examinations showed severe cardiac dilatation and fibrosis in both cases. Myocardial degeneration was observed only in the former case. Decreased (diffusion)

Enhanced calmodulin binding concurrent with increased kinase-dependent phosphorylation of cytoskeletal proteins following a single subcutaneous injection of diisopropyl phosphorofluoridate in hens.

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Diisopropyl phosphorofluoridate (DFP) produces Type I organophosphorus compound-induced delayed neurotoxicity (OPIDN) in adult female chickens. We have proposed that calcium/calmodulin protein kinase II (CaM kinase II) plays a role in the development of OPIDN by increasing the phosphorylation of

S-100 protein and calmodulin levels in cerebrospinal fluid after subarachnoid hemorrhage.

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The levels of two calcium-binding proteins, S-100 protein and calmodulin, were measured serially in the cerebrospinal fluid (CSF) of patients after subarachnoid hemorrhage (SAH) and aneurysm surgery. These two proteins have a similar molecular structure and are highly concentrated in the central

Antagonists of calmodulin delay injury development in the severely ischemic perfused working rat heart.

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The effects of calmodulin antagonists trifluoperazine (TFP) and calmidazolium (CMZ) and of ethmozine (a phenothiazine without anticalmodulin activity) on the postischemic recovery in the perfused working rat hearts were studied. In the hearts subjected to 25 min zero-flow ischemia coronary flow,

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