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	48-602MAG	Buffer Detection Kit for Magnetic Beads	1 Kit

Parotid gland involvement in advanced AIDS.
OBJECTIVE: This study describes the involvement and the histological alterations found in the parotid glands of 100 patients who died with AIDS. MATERIALS AND METHODS: Sex, age, CD4 cell count and clinical history were obtained from the files of 100 patients who died with AIDS. Histological analysis of the parotid glands was performed using HE, Gomori-Grocott, Ziehl-Neelsen and Mucicarmine. Histological findings were grouped in reactive, infectious, cystic, neoplastic and concomitant lesions. RESULTS: None of the patients presented complaints or symptoms related to salivary gland alterations prior to death. The mean age of the patients and CD4 cell count were 36.4 years and 76.07 cells microliter-1, respectively. Histological alterations of the parotid glands were found in 51% of the patients. The most common alteration was non-specific chronic sialadenitis (29 cases), followed by infectious conditions (22 cases). Mycobacteriosis was the most common infectious disease (10 cases), followed by cytomegalovirus (nine cases), cryptococcosis (three cases) and histoplasmosis (two cases). Lymphoepithelial cysts occurred in six cases, Warthin's tumor and non-Hodgkin Lymphoma in one case each. CONCLUSIONS: These results indicate that infection and other lesions in the parotid glands are more frequent than hitherto described in the specialized literature in AIDS patients. Clinicians should consider parotid gland involvement, when evaluating disease extension in advanced AIDS patients.
Document Type:

Reference

Product Catalog Number:

MAB8052
Product Catalog Name:

Anti-Adenovirus Antibody, clone 20/11
Oncogenes induce genotoxic stress by mitotic processing of unusual replication intermediates.
Oncogene-induced DNA replication stress activates the DNA damage response (DDR), a crucial anticancer barrier. DDR inactivation in these conditions promotes genome instability and tumor progression, but the underlying molecular mechanisms are elusive. We found that overexpression of both Cyclin E and Cdc25A rapidly slowed down replication forks and induced fork reversal, suggestive of increased topological stress. Surprisingly, these phenotypes, per se, are neither associated with chromosomal breakage nor with significant DDR activation. Oncogene-induced DNA breakage and DDR activation instead occurred upon persistent G2/M arrest or, in a checkpoint-defective context, upon premature CDK1 activation. Depletion of MUS81, a cell cycle-regulated nuclease, markedly limited chromosomal breakage and led to further accumulation of reversed forks. We propose that nucleolytic processing of unusual replication intermediates mediates oncogene-induced genotoxicity and that limiting such processing to mitosis is a central anti-tumorigenic function of the DNA damage checkpoints.
Document Type:

Reference

Product Catalog Number:

Multiple
Product Catalog Name:

Multiple
The role of collagen structure in mitogen stimulation of ERK, cyclin D1 expression, and G1-S progression in rat hepatocytes.
Adhesion to type 1 collagen can elicit different cellular responses dependent upon whether the collagen is in a fibrillar form (gel) or monomeric form (film). Hepatocytes adherent to collagen film spread extensively, express cyclin D1, and increase DNA synthesis in response to epidermal growth factor, whereas hepatocytes adherent to collagen gel have increased differentiated function, but lower DNA synthesis. The signaling mechanisms by which different forms of type I collagen modulate cell cycle progression are unknown. When ERK MAP kinase activation was analyzed in hepatocytes attached to collagen film, two peaks of ERK activity were demonstrated. Only the second peak, which correlated with an increase of cyclin D1, was required for G1-S progression. Notably, this second peak of ERK activity was absent in cells adherent to collagen gel, but not required in the presence of exogenous cyclin D1. Expression of activated mutants of the Ras/Raf/MEK signaling pathway in cells adherent to collagen gel restored ERK phosphorylation and DNA synthesis, but differentially affected cell shape. Although Ras, Raf, and MEK all increased expression of cyclin D1 on collagen film, only Ras and Raf significantly up-regulated cyclin D1 levels on collagen gel. These results demonstrate that adhesion to polymerized collagen induces growth arrest by inhibiting the Ras/ERK-signaling pathway to cyclin D1 required in late G1.
Document Type:

Reference

Product Catalog Number:

06-137
Regulation of G(1) cyclin-dependent kinases in the liver: role of nuclear localization and p27 sequestration.
Recent studies suggest that cyclin D1 mediates progression of hepatocytes through G(1) phase of the cell cycle. The present study further examines the regulation of cyclin D1-dependent kinase activity and the interplay between cyclin D1 and other G(1) phase regulatory proteins during liver regeneration. After 70% partial hepatectomy in rats, there was upregulation of kinase activity associated with cyclins (A, D1, D3, and E), cyclin-dependent kinases (Cdk2 and Cdk4), and Cdk-inhibitory proteins (p27, p107, and p130). Although cyclin D1/Cdk4 complexes were more abundant in the cytoplasmic fraction after partial hepatectomy, kinase activity was detected primarily in the nuclear fraction. Cytoplasmic cyclin D1/Cdk4 complexes were activated by recombinant cyclin H/Cdk7. Because endogenous Cdk7 activity was found in the nucleus, this suggests that activation of cyclin D1/Cdk4 requires nuclear importation and subsequent phosphorylation by cyclin H/Cdk7. Recombinant cyclin E/Cdk2 was inhibited by extracts from quiescent liver, and cyclin D1 could titrate out this inhibitory activity. Induction of cyclin D1 was accompanied by increased abundance of cyclin D1/p27 complexes, and most p27 was sequestered by cyclin D1 after partial hepatectomy. Thus cyclin D1 appears to play two roles during G(1) phase progression in the regenerating liver: it forms a nuclear kinase complex, and it promotes activation of Cdk2 by sequestering inhibitory proteins such as p27. These experiments underscore the complexity of cyclin/Cdk regulatory networks in the regenerating liver.
Document Type:

Reference

Product Catalog Number:

06-137

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Parotid gland involvement in advanced AIDS.

Oncogenes induce genotoxic stress by mitotic processing of unusual replication intermediates.

The role of collagen structure in mitogen stimulation of ERK, cyclin D1 expression, and G1-S progression in rat hepatocytes.

Regulation of G(1) cyclin-dependent kinases in the liver: role of nuclear localization and p27 sequestration.

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