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Brain Res. 2006 Jan 5;1067(1):170-6. Epub 2005 Dec 15.

Related Articles, Links

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Arch Insect Biochem Physiol. 2007 Apr;64(4):186-99.Click here to read  Links

Identification and expression analysis of an actin gene from the soft tick, Ornithodoros moubata (Acari: Argasidae).

P     Horigane M, Ogihara K, Nakajima Y, Honda H, Taylor D.

Graduate School of Life and Environmental Sciences, University of Tsukuba, Tsukuba Ibaraki, Japan.

Actin genes are found in all living organisms and highly conserved in various animals as shown by numerous studies on actin gene expression and function. Because of this ubiquitous nature of actin, it is often used as an internal control in gene expression studies. To clarify the suitability of actin gene as an internal control in soft ticks, isolation and expression analyses of an actin gene from Ornithodoros moubata was performed. An actin gene of Ornithodoros moubata (OmAct2, GenBank accession no. AB208021) with 1,131 bp and 376 amino acid residues was identified. The homology of OmAct2 with other arthropod actin genes was greater than 80% in nucleotides and 99% in amino acids. OmAct2 gene was classified as a cytoskeletal actin type by absence of muscle-specific amino acids commonly found in insects and ubiquitous expression in all stages and both sexes. Southern blot revealed that O. moubata has four to seven actin genes. In addition, actin expression analyzed by real-time PCR before and after blood feeding was not significantly different indicating OmAct2 is an appropriate internal control for the analysis of gene expression in these ticks. c 2007 Wiley-Liss, Inc.

PMID: 17366597 [PubMed - in process]

J Cell Biochem. 2007 Mar 28; [Epub ahead of print]Click here to read  Links

Nuclear actin is involved in the regulation of CSF1 gene transcription in a chromatin required, BRG1 independent manner.

P     Song Z, Wang M, Wang X, Pan X, Liu W, Hao S, Zeng X.

Institute of Genetics and Cytology, Northeast Normal University, Changchun 130024, China.

Actin is an important protein in nucleus and has been implicated in transcription, however, the mechanism of its function in transcription is still not clear. In this article, we studied the role of actin in the regulation of human CSF1 gene transcription. Our results showed that nuclear actin stimulates the activity of CSF1 promoter, and the role in augmenting CSF1 gene transcription requires the formation of chromatin and Z-DNA structure. The ATP binding motifs of nuclear actin are essential for its function in regulating CSF1 gene transcription, and upon actin overexpression, there is an increase in the ATPase activity of nuclear proteins. Further investigation revealed that nuclear actin regulates CSF1 gene transcription in a BRG1 independent manner. Together, these original results have provided evidence for further understanding the mechanism of nuclear actin in regulating gene transcription. J. Cell. Biochem. (c) 2007 Wiley-Liss, Inc.

PMID: 17393431 [PubMed - as supplied by publisher]

Exp Cell Res. 2007 Apr 1;313(6):1240-50. Epub 2007 Jan 31.Click here to read  Links

Regulation of TGF-beta1/MAPK-mediated PAI-1 gene expression by the actin cytoskeleton in human mesangial cells.

P     Yang C, Patel K, Harding P, Sorokin A, Glass WF 2nd.

Department of Pathology and Anatomy, Eastern Virginia Medical School, Norfolk, VA 23501, USA.

The importance of transforming growth factor-beta1 (TGF-beta1) in plasminogen activator inhibitor-1 (PAI-1) gene expression has been established, but the precise intracellular mechanisms are not fully understood. Our hypothesis is that the actin cytoskeleton is involved in TGF-beta1/MAPK-mediated PAI-1 expression in human mesangial cells. Examination of the distributions of actin filaments (F-actin), alpha-actinin, extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) by immunofluorescence and immunoprecipitation revealed that ERK and JNK associate with alpha-actinin along F-actin and that TGF-beta1 stimulation promote the dissociation of ERK and JNK with F-actin. Disassembly of the actin cytoskeleton inhibited phosphorylation of ERK and JNK and modulated PAI-1 expression and promoter activity under both basal and TGF-beta1-stimulated conditions. Stabilizing actin prevented dephosphorylation of ERK and JNK. ERK and JNK inhibitors and overexpressed dominant negative mutants antagonized the ability of TGF-beta1 to increase PAI-1 expression and promoter activity. Disassembly of F-actin also inhibited AP-1 DNA binding activity as determined by electrophoretic mobility shift assay using AP-1 consensus oligonucleotides derived from human PAI-1 promoter. F-actin stabilization prevented loss of AP-1 DNA binding activity. Therefore, changes in actin cytoskeleton modulate the ability of TGF-beta1 to stimulate PAI-1 expression through a mechanism dependent on the activation of MAPK/AP-1 pathways.

PMID: 17328891 [PubMed - in process]