Редактирование: TEAD1 (раздел)

==Publications==

{{medline-entry
|title=[Role of [[PLAT]], [[PKHD1L1]], [[STK38L]] and [[TEAD1]] genes Alu-polymorphism for longevity].
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/28556638
|abstract=The distribution of allele and genotype frequencies of Alu(I/D)-polymorphic sites in [[PLAT]] (TPA25), [[PKHD1L1]] (Yb8AC702), [[STK38L]] (Ya5ac2145) и [[TEAD1]] (Ya5ac2013) genes was first characterized in the ethnically homogeneous group (Tatars from the Republic of Bashkortostan, Russia), and was established (found) the association of each gene polymorphism with age. The study group consisted of 1580 unrelated individuals aged between 21 and 109 years, including 204 long-livers. It was found that [[STK38L]]*I/D genotype had positive association with longevity in the total group (OR=1,016, p=0,034). Long-lived women had a high probability of detection of [[PKHD1L1]]*I/I (OR=1,289, p=0,009), [[PLAT]]*D/D (OR=1,175, p=0,016) and [[TEAD1]]*I/I (OR=1,047, p=0,042) genotypes. [[PKHD1L1]]*I/D genotype was a significant factor in providing of male longevity (OR=1,713, p=0,030). Therefore, age-dependent changes in genotype frequencies are specific for each studied gene.
|mesh-terms=* Adult
* Aged
* Aged, 80 and over
* Alu Elements
* DNA-Binding Proteins
* Ethnic Groups
* Female
* Gene Frequency
* Humans
* Longevity
* Male
* Middle Aged
* Nuclear Proteins
* Polymorphism, Genetic
* Protein-Serine-Threonine Kinases
* Receptors, Cell Surface
* Russia
* Transcription Factors
|keywords=* Alu-I/D polymorphism
* PKHD1L1
* STK38L
* TEAD1
* association analysis
* gene instability
* genes of PLAT
* lifespan
* longevity
* tatars ethnic group

}}
{{medline-entry
|title=Acetylation of [[VGLL4]] Regulates Hippo-YAP Signaling and Postnatal Cardiac Growth.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27720608
|abstract=Binding of the transcriptional co-activator YAP with the transcription factor TEAD stimulates growth of the heart and other organs. YAP overexpression potently stimulates fetal cardiomyocyte (CM) proliferation, but YAP's mitogenic potency declines postnatally. While investigating factors that limit YAP's postnatal mitogenic activity, we found that the CM-enriched [[TEAD1]] binding protein [[VGLL4]] inhibits CM proliferation by inhibiting [[TEAD1]]-YAP interaction and by targeting [[TEAD1]] for degradation. Importantly, [[VGLL4]] acetylation at lysine 225 negatively regulated its binding to [[TEAD1]]. This developmentally regulated acetylation event critically governs postnatal heart growth, since overexpression of an acetylation-refractory [[VGLL4]] mutant enhanced [[TEAD1]] degradation, limited neonatal CM proliferation, and caused CM necrosis. Our study defines an acetylation-mediated, [[VGLL4]]-dependent switch that regulates TEAD stability and YAP-TEAD activity. These insights may improve targeted modulation of TEAD-YAP activity in applications from cardiac regeneration to cancer.
|mesh-terms=* Acetylation
* Adaptor Proteins, Signal Transducing
* Aging
* Amino Acid Sequence
* Animals
* Animals, Newborn
* Cell Cycle Proteins
* Cell Proliferation
* DNA-Binding Proteins
* Heart
* Heart Failure
* Humans
* Phosphoproteins
* Protein Binding
* Protein Domains
* Protein Stability
* Protein-Serine-Threonine Kinases
* Rats, Wistar
* Signal Transduction
* Transcription Factors
|keywords=* Hippo-YAP pathway
* TEAD1
* VGLL4
* acetylation
* cardiac
* cardiomyocyte
* degradation
* necrosis
* proliferation
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5121000
}}