ReviewJournal of molecular medicine (Berlin, Germany)1995
Mutations of signal-transducing G proteins in human disease.
Review in Journal of molecular medicine (Berlin, Germany), 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 15 citations in OpenAlex.
- Central precocious puberty and abnormal chromosomal patterns.Endocrine pathology · 2000Article
- Recent developments in the investigation of thyroid regulation and thyroid carcinogenesis.Environmental health perspectives · 1998Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heterotrimeric guanine nucleotide binding proteins (G proteins) couple a large number of cell surface receptors to their intracellular effector molecules, such as enzymes or ion channels. Mutations of G proteins can lead to either activation or inactivation of the corresponding signal transduction pathway and thus cause clinical symptoms. Mutations of heterotrimeric G proteins have been found in a number of endocrine tumors, the McCune-Albright syndrome, Albright's hereditary osteodystrophy, and a combination of precocious puberty and pseudohypoparathyroidism Ia. The identification of the molecular defects underlying the above disorders and the investigation of their functional consequences for metabolism and growth regulation have been the subject of many studies over the past few years. A close understanding of these pathophysiologic mechanisms is crucial for the development of therapeutic strategies.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.