| 1. |
- Kulytè, Agnè, et al.
(författare)
-
Characterization of Human Alpha-Dystrobrevin Isoforms in HL-60 Human Promyelocytic Leukemia Cells Undergoing Granulocytic Differentiation
- 2002
-
Ingår i: Molecular Biology of the Cell. - 1059-1524 .- 1939-4586. ; 13:12, s. 4195-4205
-
Tidskriftsartikel (refereegranskat)abstract
- The biochemical properties and spatial localization of the protein alpha-dystrobrevin and other isoforms were investigated in cells of the human promyelocytic leukemia line HL-60 granulocytic differentiation as induced by retinoic acid (RA). Alpha-dystrobrevin was detected both in the cytosol and the nuclei of these cells, and a short isoform (gamma-dystrobrevin) was modified by tyrosine phosphorylation soon after the onset of the RA-triggered differentiation. Varying patterns of distribution of alpha-dystrobrevin and its isoforms could be discerned in HL-60 promyelocytes, RA-differentiated mature granulocytes, and human neutrophils. Moreover, the gamma-dystrobrevin isoform was found in association with actin and myosin light chain. The results provide new information about potential involvement of alpha-dystrobrevin and its splice isoforms in signal transduction in myeloid cells during induction of granulocytic differentiation and/or at the commitment stage of differentiation or phagocytic cells.
|
|
| 2. |
- Navakauskiene, Ruta, et al.
(författare)
-
Assessment of transcription regulators and translocation of these proteins into the nucleus during granulocyte lineage commitment of haematopoietis HL-60 cells
-
Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- Expression of transcription factors required for lineage commitment of differentiating cells (C/EBPß and c-myb) and for survival of differentiated cells (STATs and NFκB) was examined in the HL-60 cell line. Differentiation was induced by treating the cells with retinoic acid (RA). c-Myb expression in the nucleus restored at the precommitment stage (18 h) what concurred with the highest nuclear level of C/EBPß, which suggests a combinatorial interaction of these transcription factors in granulocytic signalling pathway. Expression of STAT5a and STAT5b varied during differentiation; there were no significant changes in STAT3 levels. Increased cytosolic level of NFκB p65 during precommitment and commitment stages of granulocytic differentiation coincides with augmentation of STAT5a protein level what could be an evidence of their possible co-operation during granulocyticlineage commitment of HL-60 cells. Our results suggest that the studied proteins cooperatively promote signalling in differentiating promyelocytic HL-60 cell line in response to retinoic acid.
|
|
| 3. |
- Navakauskiene, Ruta, et al.
(författare)
-
Translocation of transcription regulators into the nucleus during granulocyte commitment of HL-60 cells
- 2003
-
Ingår i: Biochemistry and Cell Biology. - : Canadian Science Publishing. - 0829-8211 .- 1208-6002. ; 81:4, s. 285-295
-
Tidskriftsartikel (refereegranskat)abstract
- Expression of transcription factors required for lineage commitment of differentiating cells (C/EBPβ and c-Myb) and for survival of differentiated cells (STATs and NFκB) was examined in the HL-60 cell line. Differentiation was induced by treating the cells with retinoic acid. c-Myb expression in the nucleus restored at the precommitment stage (18 h) what concurred with the highest nuclear level of C/EBPβ, which suggests a combinatorial interaction of these transcription factors in the granulocytic signalling pathway. Expression of STAT5a and STAT5b varied during differentiation, whereas no significant changes were seen in STAT3 levels. Increased cytosolic level of NFκB p65 during precommitment and commitment stages of granulocytic differentiation coincided with augmentation of the STAT5a protein level, which could be evidence of their possible cooperation during granulocytic-lineage commitment of HL-60 cells. Our results suggest that the studied transcription factors cooperatively promote signalling in the differentiating promyelocytic HL-60 cell line in response to retinoic acid.
|
|
