High mobility group box I (HMGB1) release from tumor cells after treatment: implications for development of targeted chemoimmunotherapy.

We have recently demonstrated that cytolysis of human melanoma cells by immune effectors (both NK and T cells) is associated with release of the nuclear chromatin protein, high mobility group box I (HMGB1). Extracellular HMGB1 mediates a number of important functions including endothelial cell activation, stromagenesis, recruitment and activation of innate immune cells, and also dendritic cell maturation that, in the setting of cancer, lead to a chronic inflammatory response. This reparative inflammatory response promotes tumor cell survival, expansion, and metastases.

Neuronal control of myogenic regulatory factor accumulation in fetal muscle.

The lumbosacral spinal cords of 14.5-day gestation mice (E14.5) were ablated.

The beta-delta-core of sarcoglycan is essential for deposition at the plasma membrane.

Mutations of any of the sarcoglycan complex subunits (alpha, beta, delta, and gamma) cause limb-girdle muscular dystrophy. Furthermore, individual mutations lead to a reduction or loss of all other members of the complex. In some cases of limb-girdle muscular dystrophies, however, residual sarcoglycan expression has been documented.

Alpha-sarcoglycan is recycled from the plasma membrane in the absence of sarcoglycan complex assembly.

The sarcoglycan complex consists of four subunits in skeletal muscle (alpha, beta, gamma, and delta-SG). Mutations in alpha-sarcoglycan (alpha-SG) result in the most common form of limb girdle muscular dystrophy. However, the function of alpha-SG remains unknown.

Remodeling of vaginal connective tissue in patients with prolapse.

Objective: As pelvic organ prolapse progresses, the morphology of the vagina dramatically changes. The objective of this study was to determine whether these changes observed clinically correlate with histologic and biochemical evidence of tissue remodeling

Methods: After informed consent, full-thickness biopsies of the vaginal apex were obtained at the time of surgery from 77 women. The tissue of 15 premenopausal women with less than stage II prolapse (controls) was compared with that of 62 women with prolapse divided according to their menopausal status.

Ectopic expression of interferon regulatory factor-1 promotes human breast cancer cell death and results in reduced expression of survivin.

The overexpression of the inhibitor of apoptosis protein, survivin, may provide tumor cells with a distinct survival advantage in situ; hence, therapeutic strategies have been designed to inhibit its expression. In this study, we ectopically expressed the interferon regulatory factor (IRF)-1 protein in the breast carcinoma cell lines MDA-MB-468 and SK-BR-3 using a recombinant adenovirus (Ad-IRF-1). By screening microarray analysis of cDNA from the human breast cancer cell line MDA-MB-468 infected with Ad-IRF-1, we observed a 15-fold down-regulation of the survivin gene when compared with uninfected cells.

Effective association of Kv channel-interacting proteins with Kv4 channel is mediated with their unique core peptide.

Kv channel-interacting proteins (KChIPs) and neuronal calcium sensor-1 (NCS-1) have been shown to interact with Kv4 channel alpha-subunits to regulate the expression and/or gating of these channels. Here we examine the specificity and sites of these proteins for interaction with Kv channel proteins. Immunoprecipitation and green fluorescent protein imaging show that KChIPs (but not NCS-1) effectively bind to Kv4.