Abstracts - faqs.org

Abstracts

Biological sciences

Search abstracts:
Abstracts » Biological sciences

The neuroendocrine protein 7B2 is required for peptide hormone processing in vivo and provides a novel mechanism for pituitary Cushing's disease

Article Abstract:

The neuroendocrine protein 7B2 was examined with respect to the role it plays in the activation of prohormone convertase 2 (PC2). Using a novel transposon-based method, 7B2 null mice were generated and were discovered to lack PC2 activity. They were also found to have multiple metabolic derangements that were similar to those found in PC2 null mice. Results also showed that 7B2 null mice developed and died of Cushing's disease, with multiple sequelae of hypercorticosteronism. This seems to indicate a novel role for 7B2 in the control of peptide secretion from the pituitary gland.

Author: Schambelan, Morris, Bonner-Weir, Susan, Leder, Philip, Westphal, Christoph H., Steiner, Donald F., Muller, Laurent, Zhou, An, Zhu, Xiaorong, Lindberg, Iris
Publisher: Elsevier B.V.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1999
Laboratory animals, Endocrine gland diseases, Endocrine diseases, Corticosterone

User Contributions:

Comment about this article or add new information about this topic:

CAPTCHA


RIP: a novel protein containing a death domain that interacts with Fas/APO-1 (CD95) in yeast and causes cell death

Article Abstract:

A yeast genetic selection system identified Fas and a 74 kDa protein, designated RIP, which are two gene products that interact with the Fas cytoplasmic domain. RIP interacted weakly with the intracellular domain of TNFR1, but was susceptible to murine Ipr mutation. Overexpression of RIP caused transfected cells to undergo morphological changes characteristic of apoptosis. These results suggest that RIP induces cell death by acting as an apoptosis-inducing protein.

Author: Leder, Philip, Stanger, Ben Z., Seed, Brian, Kim, Emily, Lee, Tae-Ho
Publisher: Elsevier B.V.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1995
Yeast, Yeast (Food product)

User Contributions:

Comment about this article or add new information about this topic:

CAPTCHA


cul-1 Is required for cell cycle exit in C. elegans and identifies a novel gene family

Article Abstract:

The cul-1 gene, or cullins, belongs to a conserved family of genes that has at least five members in nematodes, six in man and three identified in budding yeast. Functional studies indicate that the gene is a regulator of the cell cycle in Caenorhabditis elegans. The expression of the cul-1 gene overrides cellular control mechanisms which regulate G1 to S-phase progression and shunts the pathway toward apoptosis.

Author: Hedgecock, Edward M., Kipreos, Edward T., Lander, Lois E., Wing, John P., He, Wei Wu
Publisher: Elsevier B.V.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1996
Genetic regulation, Cell cycle

User Contributions:

Comment about this article or add new information about this topic:

CAPTCHA


Subjects list: Research, Cell death, Cellular signal transduction
Similar abstracts:
  • Abstracts: The ATP-dependent PIM1 protease is required for the expression of intron-containing genes in mitochondria. Crystal structures of the ribosome in complex with release factors RF1 and RF2 bound to a cognate stop codon
  • Abstracts: Surface proteins of gram-positive bacteria and mechanisms of their targeting to the cell wall envelope. Cellulase, clostridia, and ethanol
  • Abstracts: Both insulin and calcium channel signaling are required for developmental regulation of serotonin synthesis in the chemosensory ADF neurons of Caenorhabditis elegans
  • Abstracts: Both insulin and calcium channel signaling are required for developmental regulation of serotonin synthesis in the chemosensory ADF neurons of Caenorhabditis elegans. part 2
  • Abstracts: The RNA-binding protein HuD: A regulator of neuronal differentiation, maintenance and plasticity. The synaptic muscle-specific kinase (MuSK) complex: New partners, new functions
This website is not affiliated with document authors or copyright owners. This page is provided for informational purposes only. Unintentional errors are possible.
Some parts © 2025 Advameg, Inc.