Hepatocellular carcinoma biomarkers, an imminent need.

Hepatocellular carcinoma (HCC) is the most common malignant neoplasm of the liver and one of the deadliest cancers worldwide. The identification of novel, highly specific and more sensitive biomarkers for HCC is crucial because existing ones are deficient and non-confirmatory without histological biopsy or imaging techniques.

Effects of neonatal maternal deprivation and postweaning environmental complexity on dendritic morphology of prefrontal pyramidal neurons in the rat.

It has been reported that periodic maternal separation in rats leads to a variety of endure behavioral, neurochemical and microstructural sequelae associated with the pathophysiology of anxiety disorders. Since it has been proposed that these changes might be permanent, we examined whether environmental complexity aid to recover the structural dendritic impairment induced by neonatal maternal deprivation in the medial prefrontal cortex of the rat. In addition, the anxiety-like behavior was assessed in the elevated plus-maze.

Chronic (-)-deprenyl administration attenuates dendritic developmental impairment induced by early social isolation in the rat.

It has been demonstrated that postweaning social isolation alters dendritic development in the medial prefrontal cortex (mPFC) of the rat. In addition, (-)-deprenyl, a monoamine oxidase B (MAO-B) inhibitor, promotes dendritic growth in prefrontocortical pyramidal cells. This study examined whether prefrontocortical dendritic developmental impairment induced by postweaning social isolation is attenuated by chronic (-)-deprenyl administration.

Effects of postweaning social isolation and re-socialization on the expression of vasoactive intestinal peptide (VIP) and dendritic development in the medial prefrontal cortex of the rat.

In the present study we evaluated the effects of early social isolation and re-socialization on dendritic development and the expression of the vasoactive intestinal peptide (VIP) in the medial prefrontal cortex (mPFC) of the rat. Sprague-Dawley male rats were reared either in isolation (IC) or social (SC) conditions from postnatal day 18 to 32. Rats were then behaviorally evaluated in the open field test, and approximately half of the animals were sacrificed.

Disruption of the actin network enhances MAP-2c and Fyn-induced process outgrowth.

We investigated the interaction of MAP-2c and Fyn in the initiation of process outgrowth in COS7 cells. Single transfections of Fyn and MAP-2c resulted in a dramatic decrease in flat, rounded COS7 cells, and a significant increase in both the number of cells with multiple short, spike-like processes, and cells with longer processes. Co-transfection of Fyn and MAP-2c resulted in an additive increase in the number of cells with more than two processes and discrete sites of co-localization within processes.

Fyn phosphorylates human MAP-2c on tyrosine 67.

The Src homology 3 (SH3) domain of Fyn binds to a conserved PXXP motif on microtubule-associated protein-2. Co-transfections into COS7 cells and in vitro kinase assays performed with Fyn and wild-type, or mutant MAP-2c, determined that Fyn phosphorylated MAP-2c on tyrosine 67. The phosphorylation generated a consensus sequence for the binding of the SH2 domain of Grb2 (pYSN).

Binding of Fyn to MAP-2c through an SH3 binding domain. Regulation of the interaction by ERK2.

Microtubule-associated protein 2 (MAP-2) isoforms are developmentally expressed in the nervous system and contain a number of functional domains. Adjacent to the first repeat of the microtubule-binding domain is an RTPPKSP motif for binding SH3 domains. To identify SH3-containing proteins that interact with MAP-2, transfections, filter overlay assays, glutathione S-transferase (GST)-mediated binding assays, co-immunoprecipitations and enzyme-linked immunosorbent assays were performed.

Expression of the fructose transporter GLUT5 in human breast cancer.

The primary metabolic characteristic of malignant cells is an increased uptake of glucose and its anaerobic metabolism. We studied the expression and function of the glucose transporters in human breast cancer cell lines and analyzed their expression in normal and neoplastic primary human breast tissue. Hexose uptake assays and immunoblotting experiments revealed that the breast carcinoma cell lines MCF-7 and MDA-468 express the glucose transporters GLUT1 and GLUT2, isoforms expressed in both normal and neoplastic breast tissue.