Wyniki wyszukiwania

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Czas wymiany doswiadczen - Dni Pola 2004

100%

Figiel M.

Wiadomości Informacje Opinie. Panorama Wsi i Rolnictwa

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2004

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nr 10

38

2

Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik

Retrograde capabilities of adeno-associated virus vectors in the central nervous system

63%

Surdyka M. M., Figiel M.

BioTechnologia. Journal of Biotechnology Computational Biology and Bionanotechnology

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2021

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tom 102

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nr 4

3

In vitro fluorescence studies of transcription factor IIB-DNA interaction

51%

Gorecki A., Figiel M., Dziedzicka-Wasylewska M.

Acta Biochimica Polonica

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2015

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tom 62

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nr 3

4

First humanized ataxin-3 knock-in mouse model presents molecular and histopathological phenotypes of spinocerebellar ataxia type 3

51%

Switonski P. M., Krzyzosiak W. J., Figiel M.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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nr Suppl.1

Spinocerebellar ataxia type 3 (SCA3) is a human neurodegenerative disorder caused by the expansion of CAG repeats in the coding region of the ataxin-3 gene. We generated the first humanized SCA3 knock-in mouse model by introducing human cDNA for ataxin-3 with 91 CAG repeats into the mouse ataxin-3 locus. The resulting animals express human mutant ataxin-3 protein in multiple brain structures and non-neuronal tissues. Like in human patients, the humanized allele shows both somatic and intergenerational CAG instability. The intergenerational instability is significantly associated with the gender of parent. Offspring inherits expanded CAG repeats in paternal transmissions and contracted CAG repeats in maternal transmissions. Moreover, mice show early upregulation of Serpina3n gene expression in the brain as early as at 7 weeks of age. This upregulation is also present in astrocytes isolated from neonatal animals, which suggest that mutant ataxin-3 has a more direct influence on a Serpina3n expression. The knock-in animals also demonstrate histopathological hallmarks of SCA3, including the damage of Purkinje cells in the cerebellum and the presence of intranuclear ataxin-3 inclusions.

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YAC128 mouse model-derived iPSCs show markers of Huntington disease

51%

Szlachcic W. J., Switonski P. M., Krzyzosiak W. J., Figiel M.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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nr Suppl.1

Huntington disease (HD) is an incurable brain disorder caused by expansion of CAG repeats in a HTT gene resulting in toxic huntingtin with long polyglutamine tract. In HD, neurons die in cerebral cortex and striatum and therefore a treatment option is a cell therapy using cells generated from induced pluripotent stem cells (iPSC) from patients. We have established a model of such therapy comprising iPSCs lines from the adult dermal fibroblasts of YAC128 HD mouse model. The cells were reprogrammed using transposable and excisable piggyBac vector expressing OSKML transcription factors. These iPSC cells show pluripotency both in in vitro (Tuj-positive neurons and beating cardiomiocytes) and in vivo (teratoma formation) differentiation assays, thus being suitable for experimental cell therapy. In addition, our YAC128/iPSC show alterations of Wnt/β-catenin and MAPK signaling pathways probably resulting from expression of human mutant huntingtin. Thus, cells suitable for cell therapy would need silencing of the mutant huntingtin. Therefore we have generated a series of therapeutic constructs based on piggyBac transposon expressing anti-huntingtin siRNAs in sh-miR backbone. We show that the construct when integrated into iPSC genome efficiently silences mutant huntingtin expression. Our platform is a useful model for investigating cell therapy outcomes in the HD mouse model.

6

Role of Wnt/Beta-catenin path way in differentiation of mouse es cells to cortical progenitors

51%

Gabka A., Krzyzosiak W. J., Figiel M.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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nr Suppl.1

The Wnt/β-catenin was reported to promote both pluripotency maintenance and differentiation. Treatment with Wnt and Nodal antagonists-Dkk1 and Lefty-1 or Wnt antagonist-IWP2 in serumfree floating culture of embryoid body-like aggregates (SFEBq) promoted ES differentiation to neural lineages with high efficiency. Surprisingly treatment with Wnt pathway agonist-Wnt3a down-regulated stem cells surface markers (GCTM2, CD9) in hES cells and evoked morphology characteristic of differentiation. We used Wnt inhibitors (iCRT3 and IWP2) and Nodal inhibitor (SB431542) alone or in combination to investigate the differentiation of mouse ES cells to cortical progenitors. SFEBq aggregates were differentiated and analyzed for the expression of the markers of cortical progenitors. The expression of Pax6, Sox1 and Foxg1 in SFEBq without inhibitors peaked on day 7 of differentiation while IWP2 and iCRT/SB431542 aggregates exhibited a delayed expression of cortical markers with highest expression on day 11 of differentiation. Moreover, the addition of Wnt3a on day 7 to 11 increased cell proliferation and sustained the expression of cortical progenitors markers. Taken together we observed an influence of Wnt regulation on neuronal differentiation and on proliferation of cells at later stage of differentiation.

7

Ancestry analysis of cows of record milk yields and its constituents

51%

Sobek Z., Rozanska-Zawieja J., Nienartowicz-Zdrojewska A., Figiel M.

Acta Scientiarum Polonorum. Zootechnica

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2012

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tom 11

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nr 4

The aim of the research was the pedigree analysis of top yielding cows. The investigation concerned the effects of male ancestors on the productivity of their female progeny. The total of 3,187 pedigrees of Holstein-Friesian cows with lifetime milk production of over 100,000 kg were examined. The cows were descendants of 971 sires. On the basis of the pedigree analysis it had been proved, that the ancestors of top yielding cows had positive effects on the productivity of their daugters, granddaughters and great-granddaughters. It had also been noted, that there were distinguished ancestors found repeatedly in the pedigrees of sires, grandsires and great-grandsires with the greatest number of high producing female descendants. The common descend of some of the champion cows explains their high productivity. The pedigree analysis had also shown, that many of them were related to one another. Looking deeper into the pedigrees of the sires we repeatedly found outstanding, high-ranking bulls. Increasing degree of relationship among many of the analysed bulls and cows may result in further increase of inbred especially in the group of the most valuable individuals.

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The effect of D380Y pathogenic mutation in human Yin Yang 1 on the protein’s structure and function

51%

Figiel M., Lakomska J., Dziedzicka-Wasylewska M., Gorecki A.

Acta Biochimica Polonica

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2020

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tom 67

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nr 1

9

Efekt krzyzowania dwu- i trojrasowego swin z udzialem rasy w.b.p., pietrain i linii p.b.bz.-23 w zakresie cech miesnosci i jakosci miesa

45%

Kocwin-Podsiadla M., Przybylski W., Kaczorek S., Krzecio E., Figiel M.

Zeszyty Naukowe. Przegląd Hodowlany

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1996

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tom 26

135-142

10

A novel approach for the in situ visualization of individual gene location within the nucleus

39%

Milewski M. C., Piasecki P., Kotkowiak W., Pasternak A., Figiel M., Figlerowicz M.

Acta Biochimica Polonica

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2018

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tom 65

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nr S2

Ograniczanie wyników

Czas wymiany doswiadczen - Dni Pola 2004

Retrograde capabilities of adeno-associated virus vectors in the central nervous system

In vitro fluorescence studies of transcription factor IIB-DNA interaction

First humanized ataxin-3 knock-in mouse model presents molecular and histopathological phenotypes of spinocerebellar ataxia type 3

YAC128 mouse model-derived iPSCs show markers of Huntington disease

Role of Wnt/Beta-catenin path way in differentiation of mouse es cells to cortical progenitors

Ancestry analysis of cows of record milk yields and its constituents

The effect of D380Y pathogenic mutation in human Yin Yang 1 on the protein’s structure and function

Efekt krzyzowania dwu- i trojrasowego swin z udzialem rasy w.b.p., pietrain i linii p.b.bz.-23 w zakresie cech miesnosci i jakosci miesa

A novel approach for the in situ visualization of individual gene location within the nucleus