More recently, a number of groups have shown how integration of intermediate molecular phenotypes, such as gene and protein expression levels, can be used to aid the reconstruction of these pathways and genes [2] [6].
It is important to point out that these cellular and molecular signatures, as well as the RA patients, represent a continuous rather than a discrete distribution, as is evident from the presence of lower inflammatory patients with intermediate molecular characteristics between these polar phenotypes.
To establish direct causal and functional associations between genotype and phenotype, it is hence indispensable to observe intermediate molecular levels, such as transcript, protein and metabolite abundance.
How cancer cells acquire a specific molecular phenotype is uncertain.
For 3-dimensional implants the retinal cell phenotype was also evaluated using Computational Molecular Phenotyping.
The cellular and molecular phenotypes of reduced RNASEH2C level were next investigated.
These tumor types have distinct molecular phenotypes [1].
Thus, on the basis of whole-mount analyses, it is possible to assign molecular phenotypes to stem (Asingle and some Apaired; GFRα1+, PLZF+, NGN3+/− and cKIT−), progenitor (some Apaired and Aaligned; GFRα1+, PLZF+, NGN3+, cKIT+/−) and differentiating (A1 A4, intermediate, B; GFRα1−, PLZF−, NGN3+ and cKIT+) spermatogonia in rodents.
Some mutations may result in combinations of these molecular phenotypes.
Alternatively, molecular phenotypes such as gene expressions are considered.
