Startsida
Hjälp
Sök i LIBRIS databas

     

 

Sökning: onr:fvnprzndcrd2fmhx > Ras-MAPK signaling ...

Ras-MAPK signaling in differentiating SH-SY5Y human neuroblastoma cells [Elektronisk resurs]

Olsson, Anna-Karin (författare)
Uppsala universitet Medicinska vetenskapsområdet (utgivare)
Publicerad: Uppsala : Acta Universitatis Upsaliensis, 2000
Engelska 66
Serie: Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, 0282-7476 0282-7476 ; 950
Läs hela texten
Läs hela texten
  • E-bokAvhandling(Diss. (sammanfattning) Uppsala : Uppsala universitet, 2000)
Sammanfattning Ämnesord
Stäng  
  • Neuroblastoma is a malignant childhood cancer, originating from sympathetic neuroblasts of the peripheral nervous system. Neuroblastoma is a heterogenous group of tumours, while some are highly malignant others can spontaneosly mature into a more benign form or regress. Less than half of the patients survive and this statistics has improved only modestly over the past 20 years. SH-SY5Y is a human neuroblastoma cell line established from a highly malignant tumour. The cells have retained a capacity to differentiate in vitro in response to low concentrations of the phorbolester 12-O-tetradecanoylphorbol-13-acetate (TPA) in the presence of serum or defined growth factors. Differentiated cells are characterised by neurite formation and upregulation of neuronal marker genes. SH-SY5Y are unresponsive to nerve growth factor (NGF), but when transfected to express the NGF-receptor TrkA, they differentiate in response to NGF. Protein kinase C (PKC) is pivotal for the differentiation response to take place. We have investigated the role of signaling through the Ras-MAPK pathway in differentiating SH-SY5Y, with respect to neurite formation, expression of neuronal marker genes and growth control. Our results show that differentiation-promoting treatment induced a sustained activation and nuclear accumulation of the MAPK ERK in SH-SY5Y. The nuclear accumulation of ERK was PKC-dependent. However, nuclear accumulation of ERK was not sufficient for a differentiation response to take place in these cells, but ERK activity was needed for the characteristic upregulation of NPY and GAP-43 induced by TPA. ERK activity did not induce neurite formation, neither was it necessary for TPA-induced neurite formation. Instead, stimulation of a pathway distinct from MEK/ERK, but downstream of Ras, was needed for morphological differentiation. We could also show that differentiated cells still entered S-phase and that there was no correlation between expression of the CKI p21 cip1 (an ERK target), BrdU-incorporation or neurite formation. 

Ämnesord

Medical and Health Sciences  (hsv)
Basic Medicine  (hsv)
Medical Genetics  (hsv)
Medicin och hälsovetenskap  (hsv)
Medicinska och farmaceutiska grundvetenskaper  (hsv)
Medicinsk genetik  (hsv)
MEDICINE  (svep)
Dermatology and venerology,clinical genetics, internal medicine  (svep)
Clinical genetics  (svep)
MEDICIN  (svep)
Dermatologi och venerologi, klinisk genetik, invärtesmedicin  (svep)
Klinisk genetik  (svep)
Pathology  (uu)
patologi  (uu)

Genre

government publication  (marcgt)

Indexterm och SAB-rubrik

Genetics
Neuroblastoma
SH-SY5Y
differentiation
neurite
Ras
MAPK
PKC
Genetik
Inställningar Hjälp

Uppgift om bibliotek saknas i LIBRIS

Kontakta ditt bibliotek, eller sök utanför LIBRIS. Se högermenyn.

Om LIBRIS
Sekretess
Hjälp
Fel i posten?
Kontakt
Teknik och format
Sök utifrån
Sökrutor
Plug-ins
Bookmarklet
Anpassa
Textstorlek
Kontrast
Vyer
LIBRIS söktjänster
SwePub
Uppsök

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

Copyright © LIBRIS - Nationella bibliotekssystem

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy