| 1. |
- Larsson, Jan-Olov, et al.
(författare)
-
Genetic and environmental contributions to stability and change of ADHD symptoms between 8 and 13 years of age : a longitudinal twin study
- 2004
-
Ingår i: Journal of the American Academy of Child and Adolescent Psychiatry. - Philadelphia, USA : Lippincott Williams & Wilkins. - 0890-8567 .- 1527-5418. ; 43:10, s. 1267-1275
-
Tidskriftsartikel (refereegranskat)abstract
- Objective: To study the genetic and environmental contributions to stability and change of attention-deficit/hyperactivity disorder (ADHD) symptoms between 8 and 9 and 13 and 14 years of age.Method: The sample included 1,480 twin pairs born in Sweden between May 1985 and December 1986. At wave 1 in 1994, when twins were 8-9 years old, 1,106 (75%) of the parents responded to a mailed questionnaire, and at wave 2 when the twins were 13-14 years old, 1,063 (73%) responded. A checklist with 14 items based on the 14 DSM-III-R symptoms for ADHD was completed. Structural equation modeling was used to analyze the data.Results: A relatively high stability of ADHD symptoms over this 5-year period was found. This continuity was mainly due to the same genetic effects operating at both points in time. Change in symptoms between childhood and early adolescence was to a large extent due to new genetic effects in early adolescence but also due to new nonshared environmental effects that became important during adolescence.Conclusions: The genetic stability highlights the importance of the continuing search for genes and endophenotypes of ADHD.
|
|
| 2. |
- Fagman, Henrik, 1975, et al.
(författare)
-
Nuclear accumulation of full-length and truncated adenomatous polyposis coli protein in tumor cells depends on proliferation.
- 2003
-
Ingår i: Oncogene. - : Springer Science and Business Media LLC. - 0950-9232 .- 1476-5594. ; 22:38, s. 6013-22
-
Tidskriftsartikel (refereegranskat)abstract
- The adenomatous polyposis coli (APC) tumor suppressor is a nucleocytoplasmic protein. The nuclear accumulation of APC was recently found to vary depending on cell density, suggesting that putative APC function(s) in the nucleus is controlled by the establishment of cell contacts. We report here that the density-dependent redistribution of APC between nucleus and cytoplasm prevails in 6/6 thyroid and colorectal carcinoma cell lines. Moreover, mutated APC lacking known nuclear localization sequences had the similar distribution pattern as the full-length protein. APC invariably accumulated in the nuclei of Ki-67 expressing cells, but was largely cytoplasmic when cell cycle exit was induced by serum starvation or at high cell density. APC colocalized with beta-catenin in the nucleus only in one cell line (SW480). Also, APC maintained a predominantly nuclear position in early confluent states when cytoplasmic beta-catenin was recruited to newly formed adherens-like junctions. The results indicate that nuclear targeting of APC is driven by cell cycle entry rather than altered cell-cell contact. The ability of C-terminally truncated APC to accumulate in the nucleus suggests that nuclear import signals other than NLS1(APC) and NLS2(APC) are functionally important. Residual function(s) of N-terminal APC fragments in tumor cells carrying APC mutations might be beneficial to tumor growth and survival.
|
|
| 3. |
- Larsson, Fredrik, 1976, et al.
(författare)
-
TSH receptor signaling via cyclic AMP inhibits cell surface degradation and internalization of E-cadherin in pig thyroid epithelium.
- 2004
-
Ingår i: Cellular and molecular life sciences : CMLS. - : Springer Science and Business Media LLC. - 1420-682X .- 1420-9071. ; 61:14, s. 1834-42
-
Tidskriftsartikel (refereegranskat)abstract
- Incorporation of E-cadherin into the adherens junction is a highly regulated process required to establish firm cell-cell adhesion in most epithelia. Less is known about the mechanisms that govern the clearance of E-cadherin from the cell surface in both normal and pathological states. In this study, we found that the steady-state removal of E-cadherin in primary cultured pig thyroid cell monolayers is slow and involves intracellular degradation. Experimental abrogation of adhesion by a Ca2+ switch induces rapid cell surface proteolysis of E-cadherin. At the same time, endocytosed intact E-cadherin and newly synthesized E-cadherin accumulate in intracellular compartments that largely escape further degradation. Acute stimulation with thyroid-stimulating hormone (TSH) or forskolin prevents all signs of accelerated E-cadherin turnover. The findings indicate that TSH receptor signaling via cyclic AMP stabilizes the assembly and retention of E-cadherin at the cell surface. This suggests a new mechanism by which TSH supports maintenance of thyroid follicular integrity.
|
|
