Wyniki wyszukiwania

1

Fosforylacja miozyny - fakty i hipotezy

100%

Kuznicki J.

Postępy Biochemii

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1989

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tom 35

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nr 3

2

Small ion and large problem - calcium and alzheimer's disease

100%

Kuznicki J.

Acta Neurobiologiae Experimentalis

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2011

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tom 71

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nr S

Alzheimer disease (AD) is one of the most common forms of dementia associated with age. It affects millions of people world-wide and there is no treatment to stop or delay its progress. The major risk factor of AD is age: statistically for 90 years old people every second will be affected. Because of a longer lifespan the number of AD patients is increasing. The disease lasts long and is devastating not only for patients, but also for the family members, who have to take 24 h care of them at later stages of the disease. All clinical trials based on the current AD hypotheses failed and some researchers predict that targeting metabolism of beta-amyloid is not the promising path to cure the disease. Thus, there is an increasing interest in searching for new potential drug targets in AD: proteins of calcium homeostasis represent some of them. Calcium signaling regulates multiple neuronal functions including synaptic transmission, plasticity and cell survival. Dysregulation of calcium homeostasis undergoes subtle changes during physiological ageing and affects neuronal function and survival. At the cellular level calcium buffering impairment, alterations in calcium entry routes into neurons, as well as mitochondrial and endoplasmic reticulum dysfunctions are observed in AD models. One of the possible targets of dysregulated calcium homeostasis in AD are proteins involved in store operated calcium entry (SOCE): Orai, calcium channel forming protein in plasma membrane and calcium sensors STIMs, located in ER. The understanding of neuronal mechanism of SOCE might help to explain the impairment of calcium homeostasis observed in AD. To identify potential drugs allowing restoring calcium homeostasis the high throughput screens are needed. We developed such screen (Honarnejad et al., abstract on AD/PD2011), which was applied to identify compounds affecting cellular calcium concentration.

3

Mozliwosci uprawy wczesnych mieszancow kukurydzy w warunkach woj. podlaskiego

100%

Kuznicki J.

Wiadomości Rolnicze. Wojewódzki Podlaski Ośrodek Doradztwa Rolniczego w Szepietowie

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2002

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nr 05

14-15

4

Występowanie, budowa i funkcja α-aktyniny

100%

Kuznicki J.

Kosmos

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1990

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tom 39

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nr 2-3

5

Role of store operated calcium entry in neurons

100%

Kuznicki J.

Acta Neurobiologiae Experimentalis

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2015

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tom 75

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nr Supl.

The number of people with neurodegenerative and psychiatric diseases is expanding globally. Unfortunately, there are no treatments, which can delay the progress of Alzheimer’s disease (AD), no new drugs with fewer side-effects on Parkinson’s disease (PD), Huntington’s disease (HD) and depression (MDD), no drugs for patients resistant to the existing MDD therapies. Moreover, in most diseases there are no reliable biomarkers for presymptomatic diagnosis and monitoring of effects of therapeutic treatments. Therefore, there is a growing need for better understanding of the basis of neurodegenerative and psychiatric diseases, identification of drug targets and new biomarkers, and development of new treatments and drugs. Altered Ca2+ homeostasis in neurons is proposed to be one of the early events responsible for AD. Disturbances in Ca2+ signaling are found in SAD patients before any obvious extracellular Aβ pathology, and Ca2+ dysfunction augments Aβ formation and Tau hyperphosphorylation. Dysregulation of Ca2+ homeostasis and signaling has been also observed in PD, HD and some psychiatric diseases. GWAS analysis identified specific SNPs in two voltage-gated calcium channels associated with a range of psychiatric disorders. We detected the enhanced magnitude of Ca2+ influx during Store Operated Calcium Entry (SOCE) in human lymphocytes from SAD patients, and decreased level of STIM2 from FAD patients in parallel to an attenuation of SOCE. The decreased level of STIM2 in AD models and brains of AD patients was confirmed by other authors. We also showed that the cytoplasmic resting Ca2+ level in cultured neurons can be modulated by overexpression of SOCE proteins (STIM1, STIM2 or Orai1). Based on our and literature data I will describe the role of SOCE in neurons and its perturbation in neurological diseases. To conclude, the SOCE proteins can be considered as new drug targets for some of these diseases and that dysregulation of SOCE might be used for diagnostic purposes.

6

Fosforylacja miozyny in vitro i in vitro. Część I. Miozyna komórek niemięśniowych

100%

Kuznicki J.

Postępy Biochemii

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1986

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tom 32

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nr 1-2

7

Udzial jonow wapnia w przekazywaniu sygnalow w jadrze komorkowym.

100%

Kuznicki J.

Postępy Biologii Komórki

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1998

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tom 25

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nr 2

311-316

8

Fosforylacja miozyny in vitro i in vitro. Część II. Miozyna mięśniowa

100%

Kuznicki J.

Postępy Biochemii

|

1986

|

tom 32

|

nr 1-2

9

Transport i funkcje jonów wapnia u eukariota

100%

Kuznicki J.

Kosmos

|

1988

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tom 37

|

nr 2

10

63%

Skibinska-Kijek A., Kuznicki J.

Acta Neurobiologiae Experimentalis

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2009

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tom 69

|

nr 3

Capacitative calcium entry (CCE) is a signifi cant component of calcium homeostasis in non-excitable cells. In neurons, an increasing number of evidence points to CCE as an important event in neuronal physiology and pathology. STIM1 is an endoplasmic reticulum (ER) residing protein, where it serves as a calcium sensor. Low level of calcium in ER drives STIM1 oligomerize and interact with plasma membrane protein Orai1, hence leading to calcium entry. Previously, we showed STIM1 expression in neurons, where it exhibits the same mode of action as described for non-excitable cells. Here we present description of STIM1 distribution in the mouse brain. The highest STIM1 immunoreactivity was observed in Purkinje neurons and their dendrites. Very high immunoreactivity was found in the basal ganglia. High immunoreactivity was present in the hippocampal formation, in the piriform cortex, also in infragranular layers and layer V pyramidal neurons in the neocortex. In amygdala most nuclei showed strong immunoreactivity, only the basolateral complex was weakly stained. The thalamus was very weakly stained, and the hypothalamus showed immunoreactivity of both cells and neuropil. Observed differences in STIM1 distribution in the brain indicates that various brain structures depends on CCE to different extend. Prominent dissimilarity of STIM1 immunoreactivity between amygdaloid nuclei is, in our opinion, the most interesting in light of anatomical and functional organization of the amygdala.

20

Mechanizmy komorkowo-specyficznej ekspresji genow - badania odcinkow promotorowych.

63%

Kuznicki J., Lesniak W.

Postępy Biologii Komórki. Suplement

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1996

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tom 07

39-54

Ograniczanie wyników

Fosforylacja miozyny - fakty i hipotezy

Small ion and large problem - calcium and alzheimer's disease

Mozliwosci uprawy wczesnych mieszancow kukurydzy w warunkach woj. podlaskiego

Występowanie, budowa i funkcja α-aktyniny

Role of store operated calcium entry in neurons

Fosforylacja miozyny in vitro i in vitro. Część I. Miozyna komórek niemięśniowych

Udzial jonow wapnia w przekazywaniu sygnalow w jadrze komorkowym.

Fosforylacja miozyny in vitro i in vitro. Część II. Miozyna mięśniowa

Transport i funkcje jonów wapnia u eukariota

Miedzynarodowy Instytut Biologii Komorkowej i Molekularnej w Warszawie. W poszukiwaniu optymalnego programu.

Aparat kurczliwy i szkieletowy komórki (Pokłosie II Międzynarodowego Kongresu Biologii Komórki)

Present and future use of isotopes as shown in studies on calcium-binding proteins

What is the function of calretinin and calcyclin in the brain?

40 lat doswiadczalnictwa terenowego w regionie poln.-wsch.