This type of disease is labeled polygenic, meaning that it requires
multiple gene combinations for expression.
It appears that the synergistic effect of
some multiple gene combinations, including Lr2BS, enhances leaf rust resistance.
Not exact matches
Standard approaches also struggle to find
combinations of
multiple genes that affect disease risk in complex ways (known as genetic interactions).
Fifty - four per cent were single
gene mutations, and the other 13 per cent were polygenic DNA variants, meaning they were a
combination of
multiple bad
genes inherited together.
One difficulty in studying the genetics of common mental illnesses is that they are generally caused by environmental factors in
combination with
multiple gene variants, any one of which usually could not by itself cause disease.
Professor Siddiqui and his team identified
multiple biological «micro-clusters» which means that there are different
combinations of active
genes in each of the reported subtypes of asthma.
This system could be used in
combination with hundreds of existing mouse strains that have been engineered to express known cancer
genes, allowing researchers to study more thoroughly the interactions of
multiple genes.
This is in accordance with previous reports that decitabine and 5 - azacytidine produce a marked synergistic effect in
combination with suberoylanilide hydroxamic acid and romidepsin in T - lymphoma cell lines by modulating cell cycle arrest and apoptosis.26, 27 As a mechanism of action, KMT2D mutations of B - lymphoma cells promote malignant outgrowth by perturbing methylation of H3K4 that affect the JAK - STAT, Toll - like receptor, or B - cell receptor pathway.28, 29 Here our study indicated that dual treatment with chidamide and decitabine enhanced the interaction of KMT2D with the transcription factor PU.1, thereby inactivating the H3K4me - associated signaling pathway MAPK, which is constitutively activated in T - cell lymphoma.13, 30,31 The transcription factor PU.1 is involved in the development of all hematopoietic lineages32 and regulates lymphoid cell growth and transformation.33 Aberrant PU.1 expression promotes acute myeloid leukemia and is related to the pathogenesis of
multiple myeloma via the MAPK pathway.34, 35 On the other hand, PU.1 is also shown to interact with chromatin remodeler and DNA methyltransferease to control hematopoiesis and suppress leukemia.36 Our data thus suggested that the combined action of chidamide and decitabine may interfere with the differentiation and / or viability of PTCL - NOS through a PU.1 - dependent
gene expression program.
For example, during T - cell development
genes encoding the TRB molecules are assembled from
multiple polymorphic
gene segments that undergo rearrangements and selection, generating Vb — Db — Jb
combinations that are unique in both length and sequence.
Here we show that pneumococcal lineages from
multiple populations each have a distinct
combination of intermediate - frequency
genes.
In most cases
multiple loci will work together so several different
genes can be used in
combination to produce a color.
A considerable genetic heterogeneity is expected within and among studies, as different
combinations of the various alleles of the
multiple genes and epistatic
gene interactions may produce similar phenotypes.