TEA consensus sequence gene transcriptions

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Associate Editor(s)-in-Chief: Henry A. Hoff

"The TEA/ATTS transcription factor family consists of mammalian, avian, nematode, insect and fungal members that share a conserved TEA domain. The TEA domain[1] represents a DNA‐binding region that is composed of 66–76 conserved amino acids (aa) in the N‐terminal section of the proteins."[2]

Human genes

Main article: Human genes

Gene expressions

Main article: Gene expressions

TEAD1

Transcriptional enhancer factor TEF-1 also known as TEA domain family member 1 (TEAD1) and transcription factor 13 (TCF-13) is a protein that in humans is encoded by the TEAD1 gene.[3][4][5][6] TEAD1 was the first member of the TEAD family of transcription factors to be identified.[3][7]

All members of the TEAD family share a highly conserved DNA binding domain called the TEA domain.[8] This DNA binding domain has a consensus DNA sequence 5’-CATTCCA/T-3’ that is called the MCAT element.[9] The three dimensional structure of the TEA domain has been identified [5]. Its conformation is close to that of the homeodomain and contains 3 α helixes (H1, H2 and H3). It is the H3 helix that enables TEAD proteins to bind DNA.[10]

Another conserved domain of TEAD1 is located at the C terminus of the protein. It allows the binding of cofactors and has been called the YAP1 binding domain, because it is its ability to bind this well-known TEAD proteins co-factor that led to its identification. Indeed, TEAD proteins cannot induce gene expression on their own. They have to associate with cofactors to be able to act[11]

TEAD1 is expressed in various tissues including skeletal muscle, pancreas, placenta, lung, and heart.[3][12][13][14][15][16][11]

TEAD2

TEAD2 (ETF, ETEF-1, TEF-4), together with TEAD1, defines a novel family of transcription factors, the TEAD family, highly conserved through evolution.[3][7] TEAD proteins were notably found in Drosophila (Scalloped), C. elegans (egl -44), S. cerevisiae and A. nidulans. TEAD2 has been less studied than TEAD1 but a few studies revealed its role during development.

TEAD2 is a member of the mammalian TEAD transcription factor family (initially named the transcriptional enhancer factor (TEF) family), which contain the TEA/ATTS DNA-binding domain.[1] Members of the family in mammals are TEAD1, TEAD2, TEAD3, TEAD4.

TEAD2 is selectively expressed in a subset of embryonic tissues including the cerebellum, testis, and distal portions of the forelimb and hindlimb buds, as well as the tail bud, but it is essentially absent from adult tissues.[14] TEAD2 has also been shown to be expressed very early during development, i.e. from the 2-cell stage.[17]

TEAD3

Transcriptional enhancer factor TEF-5 is a protein that in humans is encoded by the TEAD3 gene.[18][19][20]

This gene product is a member of the transcriptional enhancer factor (TEF) family of transcription factors, which contain the TEA/ATTS DNA-binding domain.[1] Members of the family in mammals are TEAD1, TEAD2, TEAD3, TEAD4. Transcriptional coregulators, such as WWTR1 (TAZ) bind to these transcription factors. TEAD3 is predominantly expressed in the placenta and is involved in the transactivation of the chorionic somatomammotropin-B gene enhancer. It is expressed in nervous system and muscle in fish embryos.[21] Translation of this protein is initiated at a non-AUG (AUA) start codon.[20]

TEAD4

Transcriptional enhancer factor TEF-3 is a protein that in humans is encoded by the TEAD4 gene.[4][13][22]

This gene product is a member of the transcriptional enhancer factor (TEF) family of transcription factors, which contain the TEA/ATTS DNA-binding domain.[1] Members of the family in mammals are TEAD1, TEAD2, TEAD3, TEAD4. TEAD4 is preferentially expressed in the skeletal muscle, and binds to the M-CAT regulatory element found in promoters of muscle-specific genes to direct their gene expression. Alternatively spliced transcripts encoding distinct isoforms, some of which are translated through the use of a non-AUG (UUG) initiation codon, have been described for this gene.[22] Gene ablation experiments in mice (i.e. knockout mice) showed that TEAD4 is essential for the formation of blastocysts during preimplantation embryo development.[23][24] Although it was originally hypothesized to be essential for specification of trophectoderm lineage, it was later shown that functional trophectoderm can be produced leading to formation of blastocysts under in vitro conditions that suppress oxidative stress.[25] Transcriptional coregulators, such as WWTR1 (TAZ) bind to members in this transcription factor family.

TEAD Post-transcriptional modifications

Protein Kinase A (pKA) can phosphorylate TEAD1 at serine 102, after the TEA domain. This phosphorylation is needed for the transcriptional activation of the α MyHC gene.[26] Protein Kinase C (pKC) phosphorylates TEAD1 on serine and threonine next to the last alpha loop in the TEA domain. This phosphorylation decreases TEAD1 binding to the GTIIC enhancer.[27]

TEAD1 can be palmitoylated on a conserved cysteine at the C-term of the protein. This post-translational modification is critical for proper folding of TEAD proteins and their stability.[28]

TEAD Orthologs

TEAD proteins are found in many organisms under different names, assuming different functions.

For example, in Saccharomyces cerevisiae TEC-1 regulates the transposable element TY1 and is involved in pseudohyphale growth (the elongated shape that yeasts take when grown in nutrient-poor conditions).[29]

In Aspergillus nidulans, the TEA domain protein ABAA regulates the differentiation of conidiophores.[30]

In drosophila the transcription factor Scalloped is involved in the development of the wing disc, survival and cell growth.[31]

In Xenopus laevis it has been demonstrated that the ortholog of TEAD1 regulates muscle differentiation.[32]

TEAD Functions

  • Heart development (myocardium differentiation,[33]
  • Skeletal muscle development (alpha-actin of skeletal muscles),[34][35][36])
  • Smooth muscle development (alpha-actin of smooth muscles),[34][37]
  • Regulation of myosin heavy chain genes,[38] cardiac muscular genes troponin T and I [7]
  • Regulation of proliferation,[39][40][41]
  • Regulation of apoptosis,[40][42]
  • Regulation of mouse neural development[43]
  • Neuron proliferation[12]
  • Regulation of proliferation[44]
  • Regulation of apoptosis[45]

TEAD Cofactors

TEAD proteins require cofactors to induce the transcription of target genes.[3]

TEAD interactions

TEAD1 interacts with all members of the SRC family of steroid receptor coactivators. In HeLa cells TEAD1 and SRC induce gene expression,[46] TEAD1 interacts with PARP (Poly-ADP ribose polymerase) to regulate smooth muscle α-actin expression. PARP can also ADP-ribosylate the TEAD proteins and make the chromatin context favorable to transcription through histone modification,[47] SRF (Serum response factor) and TEAD1 together regulate gene expression.[48]

TEAD proteins and MEF2 (myocyte enhancer factor 2) interact physically. The binding of MEF2 on DNA induces and potentiates TEAD1 recruitment at MCAT sequences that are adjacent to MEF2 binding sites. This recruitment leads to the repression of the MLC2v (Myosin Light Chain 2 v) and βMHC ( β-myosin heavy chain ) promoter.[49] TEAD1 and the phosphoprotein MAX interact in vivo and in vitro. Once this complex is formed, these two proteins can regulate the alpha-myosin heavy chain (α-MHC) gene expression.[50]

The four Vestigial-like (VGLL) proteins are able to interact with all TEADs.[51] The precise function of TEAD and VGLL interaction is still poorly understood. It has been shown that TEAD/VGLL1 complexes promote anchorage-independent cell proliferation in prostate cancer cell lines suggesting a role in cancer progression[52] Moreover, VGLL2 interaction with TEAD1 activates muscle promoter upon C2C12 differentiation and enhances MyoD-mediated myogenic in 10T1/2.[53] Finally the complex TEAD/VGLL4 acts as a default transcriptional repressor.[54]

The interaction between YAP (Yes Associated Protein 65), TAZ, a transcriptional coactivator paralog to YAP, and all TEAD proteins was demonstrated both in vitro and in vivo. In both cases the interaction of the proteins leads to increased TEAD transcriptional activity.[54][55] YAP/TAZ are effectors of the Hippo tumor suppressor pathway that restricts organ growth by keeping in check cell proliferation and promoting apoptosis in mammals and also in Drosophila.[39][41]

Cancers

Analysis of cancer transcriptome databases (www.ebi.ac.uk/gxa) showed that TEAD1 is dysregulated in several types of cancers. First in Kaposi sarcoma there is a 300-fold increase in TEAD1 levels. Moreover, the increase of TEAD expression can be detected in basal-like breast cancers,[56][57] fallopian tube carcinoma,[58] and germ cell tumors.[59] Otherwise, in other types of cancer TEAD expression is decreased, for example in other breast cancer types and in renal or bladder cancers. This dual role can be explained by the different targets and the differential regulation of target genes by TEAD transcription factors.[40][60] Finally recent studies showed that TEAD1 and YAP in ovarian cancer can induces cell stemness and chemoresistance.[61] and that genetic variant of TEAD protein and YAP are enriched in some cancers.[62]

Recent animal models indicating a possible association of TEAD2 with anencephaly.[43]

Consensus sequences

Main article: Consensus sequence gene transcriptions

"The TEA consensus sequence (TCS) in a fungal TEA/ATTS transcription factor target promoter has been defined as 5′‐CATTCY‐3′ (Andrianopoulos and Timberlake, 1994)."[2]

Binding site for

Enhancer activity

Main article: Enhancer activity copy gene transcriptions

Promoter occurrences

Main article: Promoter occurrence gene transcriptions

Hypotheses

Main article: Hypotheses
  1. A1BG has no regulatory elements in either promoter.
  2. A1BG is not transcribed by a regulatory element.
  3. No regulatory element participates in the transcription of A1BG.

TEA samplings

Main article: Model samplings

Copying a responsive elements consensus sequence CATTC(C/T) and putting the sequence in "⌘F" finds three between ZNF497 and A1BG or 2 between ZSCAN22 and A1BG as can be found by the computer programs.

For the Basic programs testing consensus sequence CATTC(C/T) (starting with SuccessablesTEA.bas) written to compare nucleotide sequences with the sequences on either the template strand (-), or coding strand (+), of the DNA, in the negative direction (-), or the positive direction (+), the programs are, are looking for, and found:

  1. negative strand, negative direction, looking for CATTC(C/T), 2, CATTCT at 3893, CATTCT at 2503.
  2. positive strand, negative direction, looking for CATTC(C/T), 0.
  3. positive strand, positive direction, looking for CATTC(C/T), 1, CATTCC at 2457.
  4. negative strand, positive direction, looking for CATTC(C/T), 2, CATTCT at 3074, CATTCC at 2208.
  1. inverse complement, negative strand, negative direction, looking for (A/G)GAATG, 0.
  2. inverse complement, positive strand, negative direction, looking for (A/G)GAATG, 3, GGAATG at 4554, AGAATG at 3003, AGAATG at 1947.
  3. inverse complement, positive strand, positive direction, looking for (A/G)GAATG, 2, AGAATG at 1887, AGAATG at 523.
  4. inverse complement, negative strand, positive direction, looking for (A/G)GAATG, 8, AGAATG at 3834, GGAATG at 3566, GGAATG at 3440, GGAATG at 3366, AGAATG at 3068, AGAATG at 2840, AGAATG at 1419, AGAATG at 1319.

TEA (4560-2846) UTRs

  1. Negative strand, negative direction: CATTCT at 3893.
  2. Positive strand, negative direction: GGAATG at 4554, AGAATG at 3003.

TEA negative direction (2596-1) distal promoters

  1. Negative strand, negative direction: CATTCT at 2503.
  2. Positive strand, negative direction: AGAATG at 1947.

TEA positive direction (4050-1) distal promoters

  1. Negative strand, positive direction: CATTCT at 3074, CATTCC at 2208.
  2. Negative strand, positive direction: AGAATG at 3834, GGAATG at 3566, GGAATG at 3440, GGAATG at 3366, AGAATG at 3068, AGAATG at 2840, AGAATG at 1419, AGAATG at 1319.
  3. Positive strand, positive direction: CATTCC at 2457.
  4. Positive strand, positive direction: AGAATG at 1887, AGAATG at 523.

TEA random dataset samplings

  1. TEAr0: 4, CATTCC at 3390, CATTCC at 3050, CATTCT at 1267, CATTCT at 891.
  2. TEAr1: 3, CATTCT at 2295, CATTCT at 1318, CATTCC at 774.
  3. TEAr2: 2, CATTCT at 1638, CATTCC at 116.
  4. TEAr3: 5, CATTCC at 3472, CATTCC at 3088, CATTCC at 2348, CATTCC at 1461, CATTCC at 481.
  5. TEAr4: 4, CATTCC at 3700, CATTCC at 2113, CATTCC at 1552, CATTCT at 310.
  6. TEAr5: 1, CATTCC at 3823.
  7. TEAr6: 3, CATTCT at 3999, CATTCC at 3690, CATTCC at 984.
  8. TEAr7: 3, CATTCT at 2272, CATTCT at 1946, CATTCT at 1018.
  9. TEAr8: 1, CATTCT at 1281.
  10. TEAr9: 2, CATTCC at 3660, CATTCT at 3103.
  11. TEAr0ci: 2, GGAATG at 1897, AGAATG at 934.
  12. TEAr1ci: 1, AGAATG at 2269.
  13. TEAr2ci: 2, GGAATG at 4492, GGAATG at 4356.
  14. TEAr3ci: 1, AGAATG at 4316.
  15. TEAr4ci: 2, GGAATG at 2701, AGAATG at 1100.
  16. TEAr5ci: 5, AGAATG at 4340, AGAATG at 3530, GGAATG at 3185, GGAATG at 2340, AGAATG at 502.
  17. TEAr6ci: 1, AGAATG at 993.
  18. TEAr7ci: 2, AGAATG at 1643, GGAATG at 103.
  19. TEAr8ci: 4, AGAATG at 2648, GGAATG at 2536, AGAATG at 1295, GGAATG at 157.
  20. TEAr9ci: 4, AGAATG at 4412, GGAATG at 3677, AGAATG at 2462, GGAATG at 2230.

TEAr arbitrary (evens) (4560-2846) UTRs

  1. TEAr0: CATTCC at 3390, CATTCC at 3050.
  2. TEAr4: CATTCC at 3700.
  3. TEAr6: CATTCT at 3999, CATTCC at 3690.
  4. TEAr2ci: GGAATG at 4492, GGAATG at 4356.

TEAr alternate (odds) (4560-2846) UTRs

  1. TEAr3: CATTCC at 3472, CATTCC at 3088.
  2. TEAr5: CATTCC at 3823.
  3. TEAr9: CATTCC at 3660, CATTCT at 3103.
  4. TEAr3ci: AGAATG at 4316.
  5. TEAr5ci: AGAATG at 4340, AGAATG at 3530, GGAATG at 3185.
  6. TEAr9ci: AGAATG at 4412, GGAATG at 3677.

TEAr arbitrary positive direction (odds) (4445-4265) core promoters

  1. TEAr3ci: AGAATG at 4316.
  2. TEAr5ci: AGAATG at 4340.
  3. TEAr9ci: AGAATG at 4412.

TEAr alternate positive direction (evens) (4445-4265) core promoters

  1. TEAr2ci: GGAATG at 4356.

TEAr arbitrary negative direction (evens) (2811-2596) proximal promoters

  1. TEAr4ci: GGAATG at 2701.
  2. TEAr8ci: AGAATG at 2648.

TEAr arbitrary negative direction (evens) (2596-1) distal promoters

  1. TEAr0: CATTCT at 1267, CATTCT at 891.
  2. TEAr2: CATTCT at 1638, CATTCC at 116.
  3. TEAr4: CATTCC at 2113, CATTCC at 1552, CATTCT at 310.
  4. TEAr6: CATTCC at 984.
  5. TEAr8: CATTCT at 1281.
  6. TEAr0ci: GGAATG at 1897, AGAATG at 934.
  7. TEAr4ci: AGAATG at 1100.
  8. TEAr6ci: AGAATG at 993.
  9. TEAr8ci: GGAATG at 2536, AGAATG at 1295, GGAATG at 157.

TEAr alternate negative direction (odds) (2596-1) distal promoters

  1. TEAr1: CATTCT at 2295, CATTCT at 1318, CATTCC at 774.
  2. TEAr3: CATTCC at 2348, CATTCC at 1461, CATTCC at 481.
  3. TEAr7: CATTCT at 2272, CATTCT at 1946, CATTCT at 1018.
  4. TEAr1ci: AGAATG at 2269.
  5. TEAr5ci: GGAATG at 2340, AGAATG at 502.
  6. TEAr7ci: AGAATG at 1643, GGAATG at 103.
  7. TEAr9ci: AGAATG at 2462, GGAATG at 2230.

TEAr arbitrary positive direction (odds) (4050-1) distal promoters

  1. TEAr1: CATTCT at 2295, CATTCT at 1318, CATTCC at 774.
  2. TEAr3: CATTCC at 3472, CATTCC at 3088, CATTCC at 2348, CATTCC at 1461, CATTCC at 481.
  3. TEAr5: CATTCC at 3823.
  4. TEAr7: CATTCT at 2272, CATTCT at 1946, CATTCT at 1018.
  5. TEAr9: CATTCC at 3660, CATTCT at 3103.
  6. TEAr1ci: AGAATG at 2269.
  7. TEAr5ci: AGAATG at 3530, GGAATG at 3185, GGAATG at 2340, AGAATG at 502.
  8. TEAr7ci: AGAATG at 1643, GGAATG at 103.
  9. TEAr9ci: GGAATG at 3677, AGAATG at 2462, GGAATG at 2230.

TEAr alternate positive direction (evens) (4050-1) distal promoters

  1. TEAr0: CATTCC at 3390, CATTCC at 3050, CATTCT at 1267, CATTCT at 891.
  2. TEAr2: CATTCT at 1638, CATTCC at 116.
  3. TEAr4: CATTCC at 3700, CATTCC at 2113, CATTCC at 1552, CATTCT at 310.
  4. TEAr6: CATTCT at 3999, CATTCC at 3690, CATTCC at 984.
  5. TEAr8: CATTCT at 1281.
  6. TEAr0ci: GGAATG at 1897, AGAATG at 934.
  7. TEAr4ci: GGAATG at 2701, AGAATG at 1100.
  8. TEAr6ci: AGAATG at 993.
  9. TEAr8ci: AGAATG at 2648, GGAATG at 2536, AGAATG at 1295, GGAATG at 157.

TEA analysis and results

Main article: Complex locus A1BG and ZNF497 § TEAs

"The TEA consensus sequence (TCS) in a fungal TEA/ATTS transcription factor target promoter has been defined as 5′‐CATTCY‐3′ (Andrianopoulos and Timberlake, 1994)."[2]

Reals or randoms Promoters direction Numbers Strands Occurrences Averages (± 0.1)
Reals UTR negative 3 2 1.5 1.5 ± 0.5 (--1,+-2)
Randoms UTR arbitrary negative 7 10 0.7 0.9 ± 0.2 (7,11)
Randoms UTR alternate negative 11 10 1.1 0.9 ± 0.2 (7,11)
Reals Core negative 0 2 0 0
Randoms Core arbitrary negative 0 10 0 0
Randoms Core alternate negative 0 10 0 0
Reals Core positive 0 2 0 0
Randoms Core arbitrary positive 3 10 0.3 0.2 ± 0.1
Randoms Core alternate positive 1 10 0.1 0.2 ± 0.1
Reals Proximal negative 0 2 0 0
Randoms Proximal arbitrary negative 2 10 0.2 0.1
Randoms Proximal alternate negative 0 10 0 0.1
Reals Proximal positive 0 2 0 0
Randoms Proximal arbitrary positive 0 10 0 0
Randoms Proximal alternate positive 0 10 0 0
Reals Distal negative 2 2 1 1 ± 0 (--1,+-1)
Randoms Distal arbitrary negative 16 10 1.6 1.6
Randoms Distal alternate negative 16 10 1.6 1.6
Reals Distal positive 13 2 6.5 6.5 ± 3.5 (-+10,++3)
Randoms Distal arbitrary positive 24 10 2.4 2.35 ± 0.05
Randoms Distal alternate positive 23 10 2.3 2.35 ± 0.05

Comparison:

The occurrences of real TEA UTRs overlap high randoms, positive distals are greater than the randoms, negative distals are less than the randoms. This suggests that the real TEAs are likely active or activable.

Acknowledgements

The content on this page was first contributed by: Henry A. Hoff.

See also

References

  1. ↑ 1.0 1.1 1.2 1.3 Bürglin TR (July 1991). "The TEA domain: a novel, highly conserved DNA-binding motif". Cell. 66 (1): 11–2. doi:10.1016/0092-8674(91)90132-I. PMID 2070413. Unknown parameter |s2cid= ignored (help)
  2. ↑ 2.0 2.1 2.2 Anja Schweizer, Steffen Rupp, Brad N. Taylor, Martin Röllinghoff, Klaus Schröppel (November 2000). "The TEA/ATTS transcription factor CaTec1p regulates hyphal development and virulence in Candida albicans". Molecular Microbiology. 38 (3): 435–445. doi:10.1046/j.1365-2958.2000.02132.x. Retrieved 21 April 2021.
  3. ↑ 3.0 3.1 3.2 3.3 3.4 Xiao JH, Davidson I, Matthes H, Garnier JM, Chambon P (May 1991). "Cloning, expression, and transcriptional properties of the human enhancer factor TEF-1". Cell. 65 (4): 551–68. doi:10.1016/0092-8674(91)90088-G. PMID 1851669. Unknown parameter |s2cid= ignored (help)
  4. ↑ 4.0 4.1 Jacquemin P, Depetris D, Mattei MG, Martial JA, Davidson I (January 1999). "Localization of human transcription factor TEF-4 and TEF-5 (TEAD2, TEAD3) genes to chromosomes 19q13.3 and 6p21.2 using fluorescence in situ hybridization and radiation hybrid analysis". Genomics. 55 (1): 127–9. doi:10.1006/geno.1998.5628. hdl:2268/13836. PMID 9889009.
  5. ↑ Fossdal R, Jonasson F, Kristjansdottir GT, Kong A, Stefansson H, Gosh S, Gulcher JR, Stefansson K (May 2004). "A novel TEAD1 mutation is the causative allele in Sveinsson's chorioretinal atrophy (helicoid peripapillary chorioretinal degeneration)". Human Molecular Genetics. 13 (9): 975–81. doi:10.1093/hmg/ddh106. PMID 15016762.
  6. ↑ "Entrez Gene: TEAD1 TEA domain family member 1 (SV40 transcriptional enhancer factor)".
  7. ↑ 7.0 7.1 7.2 Mar JH, Ordahl CP (September 1988). "A conserved CATTCCT motif is required for skeletal muscle-specific activity of the cardiac troponin T gene promoter". Proceedings of the National Academy of Sciences of the United States of America. 85 (17): 6404–8. Bibcode:1988PNAS...85.6404M. doi:10.1073/pnas.85.17.6404. PMC 281980. PMID 3413104.
  8. ↑ Hwang JJ, Chambon P, Davidson I (June 1993). "Characterization of the transcription activation function and the DNA binding domain of transcriptional enhancer factor-1". The EMBO Journal. 12 (6): 2337–48. doi:10.1002/j.1460-2075.1993.tb05888.x. PMC 413464. PMID 8389695.
  9. ↑ Farrance IK, Mar JH, Ordahl CP (August 1992). "M-CAT binding factor is related to the SV40 enhancer binding factor, TEF-1". The Journal of Biological Chemistry. 267 (24): 17234–40. doi:10.1016/S0021-9258(18)41917-5. PMID 1324927.
  10. ↑ Anbanandam A, Albarado DC, Nguyen CT, Halder G, Gao X, Veeraraghavan S (November 2006). "Insights into transcription enhancer factor 1 (TEF-1) activity from the solution structure of the TEA domain". Proceedings of the National Academy of Sciences of the United States of America. 103 (46): 17225–30. Bibcode:2006PNAS..10317225A. doi:10.1073/pnas.0607171103. PMC 1859914. PMID 17085591.
  11. ↑ 11.0 11.1 Azakie A, Lamont L, Fineman JR, He Y (December 2005). "Divergent transcriptional enhancer factor-1 regulates the cardiac troponin T promoter". American Journal of Physiology. Cell Physiology. 289 (6): C1522–34. doi:10.1152/ajpcell.00126.2005. PMID 16049055.
  12. ↑ 12.0 12.1 Jacquemin P, Hwang JJ, Martial JA, Dollé P, Davidson I (September 1996). "A novel family of developmentally regulated mammalian transcription factors containing the TEA/ATTS DNA binding domain". The Journal of Biological Chemistry. 271 (36): 21775–85. doi:10.1074/jbc.271.36.21775. PMID 8702974.
  13. ↑ 13.0 13.1 Stewart AF, Richard CW, Suzow J, Stephan D, Weremowicz S, Morton CC, Adra CN (October 1996). "Cloning of human RTEF-1, a transcriptional enhancer factor-1-related gene preferentially expressed in skeletal muscle: evidence for an ancient multigene family". Genomics. 37 (1): 68–76. doi:10.1006/geno.1996.0522. PMID 8921372.
  14. ↑ 14.0 14.1 Yasunami M, Suzuki K, Houtani T, Sugimoto T, Ohkubo H (August 1995). "Molecular characterization of cDNA encoding a novel protein related to transcriptional enhancer factor-1 from neural precursor cells". The Journal of Biological Chemistry. 270 (31): 18649–54. doi:10.1074/jbc.270.31.18649. PMID 7629195.
  15. ↑ Yasunami M, Suzuki K, Ohkubo H (November 1996). "A novel family of TEA domain-containing transcription factors with distinct spatiotemporal expression patterns". Biochemical and Biophysical Research Communications. 228 (2): 365–70. doi:10.1006/bbrc.1996.1667. PMID 8920920.
  16. ↑ Yockey CE, Smith G, Izumo S, Shimizu N (February 1996). "cDNA cloning and characterization of murine transcriptional enhancer factor-1-related protein 1, a transcription factor that binds to the M-CAT motif". The Journal of Biological Chemistry. 271 (7): 3727–36. doi:10.1074/jbc.271.7.3727. PMID 8631987.
  17. ↑ Kaneko KJ, Cullinan EB, Latham KE, DePamphilis ML (May 1997). "Transcription factor mTEAD-2 is selectively expressed at the beginning of zygotic gene expression in the mouse". Development. 124 (10): 1963–73. doi:10.1242/dev.124.10.1963. PMID 9169843.
  18. ↑ Jacquemin P, Depetris D, Mattei MG, Martial JA, Davidson I (January 1999). "Localization of human transcription factor TEF-4 and TEF-5 (TEAD2, TEAD3) genes to chromosomes 19q13.3 and 6p21.2 using fluorescence in situ hybridization and radiation hybrid analysis". Genomics. 55 (1): 127–9. doi:10.1006/geno.1998.5628. hdl:2268/13836. PMID 9889009.
  19. ↑ Jacquemin P, Martial JA, Davidson I (May 1997). "Human TEF-5 is preferentially expressed in placenta and binds to multiple functional elements of the human chorionic somatomammotropin-B gene enhancer". The Journal of Biological Chemistry. 272 (20): 12928–37. doi:10.1074/jbc.272.20.12928. PMID 9148898.
  20. ↑ 20.0 20.1 "Entrez Gene: TEAD3 TEA domain family member 3".
  21. ↑ Mann CJ, Osborn DP, Hughes SM (Oct 2007). "Vestigial-like-2b (VITO-1b) and Tead-3a (Tef-5a) expression in zebrafish skeletal muscle, brain and notochord". Gene Expression Patterns. 7 (8): 827–36. doi:10.1016/j.modgep.2007.08.001. PMC 3360971. PMID 17916448.
  22. ↑ 22.0 22.1 "Entrez Gene: TEAD4 TEA domain family member 4".
  23. ↑ Yagi R, Kohn MJ, Karavanova I, Kaneko KJ, Vullhorst D, DePamphilis ML, Buonanno A (November 2007). "Transcription factor TEAD4 specifies the trophectoderm lineage at the beginning of mammalian development". Development. 134 (21): 3827–36. doi:10.1242/dev.010223. PMID 17913785.
  24. ↑ Nishioka N, Yamamoto S, Kiyonari H, Sato H, Sawada A, Ota M, Nakao K, Sasaki H (2008). "Tead4 is required for specification of trophectoderm in pre-implantation mouse embryos". Mechanisms of Development. 125 (3–4): 270–83. doi:10.1016/j.mod.2007.11.002. PMID 18083014. Unknown parameter |s2cid= ignored (help)
  25. ↑ Kaneko KJ, DePamphilis ML (September 2013). "TEAD4 establishes the energy homeostasis essential for blastocoel formation". Development. 140 (17): 3680–90. doi:10.1242/dev.093799. PMC 3742148. PMID 23903192.
  26. ↑ Gupta MP, Gupta M, Dizon E, Zak R (1996). "Sympathetic control of cardiac myosin heavy chain gene expression". Molecular and Cellular Biochemistry. 157 (1–2): 117–24. doi:10.1007/bf00227889. PMID 8739237. Unknown parameter |s2cid= ignored (help)
  27. ↑ Jiang SW, Dong M, Trujillo MA, Miller LJ, Eberhardt NL (June 2001). "DNA binding of TEA/ATTS domain factors is regulated by protein kinase C phosphorylation in human choriocarcinoma cells". The Journal of Biological Chemistry. 276 (26): 23464–70. doi:10.1074/jbc.M010934200. PMID 11313339.
  28. ↑ Noland CL, Gierke S, Schnier PD, Murray J, Sandoval WN, Sagolla M, Dey A, Hannoush RN, Fairbrother WJ, Cunningham CN (January 2016). "Palmitoylation of TEAD Transcription Factors Is Required for Their Stability and Function in Hippo Pathway Signaling". Structure. 24 (1): 179–86. doi:10.1016/j.str.2015.11.005. PMID 26724994.
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  32. ↑ Naye F, Tréguer K, Soulet F, Faucheux C, Fédou S, Thézé N, Thiébaud P (2007). "Differential expression of two TEF-1 (TEAD) genes during Xenopus laevis development and in response to inducing factors". The International Journal of Developmental Biology. 51 (8): 745–52. doi:10.1387/ijdb.072375fn. PMID 17939122.
  33. ↑ Chen Z, Friedrich GA, Soriano P (October 1994). "Transcriptional enhancer factor 1 disruption by a retroviral gene trap leads to heart defects and embryonic lethality in mice". Genes & Development. 8 (19): 2293–301. doi:10.1101/gad.8.19.2293. PMID 7958896.
  34. ↑ 34.0 34.1 Jiang SW, Trujillo MA, Sakagashira M, Wilke RA, Eberhardt NL (March 2000). "Novel human TEF-1 isoforms exhibit altered DNA binding and functional properties". Biochemistry. 39 (12): 3505–13. doi:10.1021/bi991048w. PMID 10727247.
  35. ↑ Karns LR, Kariya K, Simpson PC (January 1995). "M-CAT, CArG, and Sp1 elements are required for alpha 1-adrenergic induction of the skeletal alpha-actin promoter during cardiac myocyte hypertrophy. Transcriptional enhancer factor-1 and protein kinase C as conserved transducers of the fetal program in cardiac growth". The Journal of Biological Chemistry. 270 (1): 410–7. doi:10.1074/jbc.270.1.410. PMID 7814403.
  36. ↑ Benhaddou A, Keime C, Ye T, Morlon A, Michel I, Jost B, Mengus G, Davidson I (February 2012). "Transcription factor TEAD4 regulates expression of myogenin and the unfolded protein response genes during C2C12 cell differentiation". Cell Death and Differentiation. 19 (2): 220–31. doi:10.1038/cdd.2011.87. PMC 3263497. PMID 21701496.
  37. ↑ Swartz EA, Johnson AD, Owens GK (August 1998). "Two MCAT elements of the SM alpha-actin promoter function differentially in SM vs. non-SM cells". The American Journal of Physiology. 275 (2 Pt 1): C608–18. doi:10.1152/ajpcell.1998.275.2.C608. PMID 9688616.
  38. ↑ Rindt H, Gulick J, Knotts S, Neumann J, Robbins J (March 1993). "In vivo analysis of the murine beta-myosin heavy chain gene promoter". The Journal of Biological Chemistry. 268 (7): 5332–8. doi:10.1016/S0021-9258(18)53537-7. PMID 8444907.
  39. ↑ 39.0 39.1 Yu FX, Zhao B, Guan KL (November 2015). "Hippo Pathway in Organ Size Control, Tissue Homeostasis, and Cancer". Cell. 163 (4): 811–28. doi:10.1016/j.cell.2015.10.044. PMC 4638384. PMID 26544935.
  40. ↑ 40.0 40.1 40.2 Landin Malt A, Cagliero J, Legent K, Silber J, Zider A, Flagiello D (2012). "Alteration of TEAD1 expression levels confers apoptotic resistance through the transcriptional up-regulation of Livin". PLOS ONE. 7 (9): e45498. Bibcode:2012PLoSO...745498L. doi:10.1371/journal.pone.0045498. PMC 3454436. PMID 23029054.
  41. ↑ 41.0 41.1 Zhao B, Li L, Lei Q, Guan KL (May 2010). "The Hippo-YAP pathway in organ size control and tumorigenesis: an updated version". Genes & Development. 24 (9): 862–74. doi:10.1101/gad.1909210. PMC 2861185. PMID 20439427.
  42. ↑ Landin Malt A, Georges A, Silber J, Zider A, Flagiello D (October 2013). "Interaction with the Yes-associated protein (YAP) allows TEAD1 to positively regulate NAIP expression". FEBS Letters. 587 (19): 3216–23. doi:10.1016/j.febslet.2013.08.013. PMID 23994529. Unknown parameter |s2cid= ignored (help)
  43. ↑ 43.0 43.1 Kaneko KJ, Kohn MJ, Liu C, DePamphilis ML (September 2007). "Transcription factor TEAD2 is involved in neural tube closure". Genesis. 45 (9): 577–87. doi:10.1002/dvg.20330. PMC 2765819. PMID 17868131.
  44. ↑ Sawada A, Kiyonari H, Ukita K, Nishioka N, Imuta Y, Sasaki H (May 2008). "Redundant roles of Tead1 and Tead2 in notochord development and the regulation of cell proliferation and survival". Molecular and Cellular Biology. 28 (10): 3177–89. doi:10.1128/MCB.01759-07. PMC 2423158. PMID 18332127.
  45. ↑ Sawada A, Kiyonari H, Ukita K, Nishioka N, Imuta Y, Sasaki H (May 2008). "Redundant roles of Tead1 and Tead2 in notochord development and the regulation of cell proliferation and survival". Molecular and Cellular Biology. 28 (10): 3177–89. doi:10.1128/MCB.01759-07. PMC 2423158. PMID 18332127.
  46. ↑ Belandia B, Parker MG (October 2000). "Functional interaction between the p160 coactivator proteins and the transcriptional enhancer factor family of transcription factors". The Journal of Biological Chemistry. 275 (40): 30801–5. doi:10.1074/jbc.C000484200. PMID 10934189.
  47. ↑ Butler AJ, Ordahl CP (January 1999). "Poly(ADP-ribose) polymerase binds with transcription enhancer factor 1 to MCAT1 elements to regulate muscle-specific transcription". Molecular and Cellular Biology. 19 (1): 296–306. doi:10.1128/mcb.19.1.296. PMC 83887. PMID 9858553.
  48. ↑ MacLellan WR, Lee TC, Schwartz RJ, Schneider MD (June 1994). "Transforming growth factor-beta response elements of the skeletal alpha-actin gene. Combinatorial action of serum response factor, YY1, and the SV40 enhancer-binding protein, TEF-1". The Journal of Biological Chemistry. 269 (24): 16754–60. doi:10.1016/S0021-9258(19)89455-3. PMID 8206998.
  49. ↑ Maeda T, Chapman DL, Stewart AF (December 2002). "Mammalian vestigial-like 2, a cofactor of TEF-1 and MEF2 transcription factors that promotes skeletal muscle differentiation". The Journal of Biological Chemistry. 277 (50): 48889–98. doi:10.1074/jbc.M206858200. PMID 12376544.
  50. ↑ Gupta MP, Amin CS, Gupta M, Hay N, Zak R (July 1997). "Transcription enhancer factor 1 interacts with a basic helix-loop-helix zipper protein, Max, for positive regulation of cardiac alpha-myosin heavy-chain gene expression". Molecular and Cellular Biology. 17 (7): 3924–36. doi:10.1128/mcb.17.7.3924. PMC 232245. PMID 9199327.
  51. ↑ Chen L, Chan SW, Zhang X, Walsh M, Lim CJ, Hong W, Song H (February 2010). "Structural basis of YAP recognition by TEAD4 in the hippo pathway". Genes & Development. 24 (3): 290–300. doi:10.1101/gad.1865310. PMC 2811830. PMID 20123908.
  52. ↑ Pobbati AV, Chan SW, Lee I, Song H, Hong W (July 2012). "Structural and functional similarity between the Vgll1-TEAD and the YAP-TEAD complexes". Structure. 20 (7): 1135–40. doi:10.1016/j.str.2012.04.004. PMID 22632831.
  53. ↑ Günther S, Mielcarek M, Krüger M, Braun T (2004). "VITO-1 is an essential cofactor of TEF1-dependent muscle-specific gene regulation". Nucleic Acids Research. 32 (2): 791–802. doi:10.1093/nar/gkh248. PMC 373362. PMID 14762206.
  54. ↑ 54.0 54.1 Koontz LM, Liu-Chittenden Y, Yin F, Zheng Y, Yu J, Huang B, Chen Q, Wu S, Pan D (May 2013). "The Hippo effector Yorkie controls normal tissue growth by antagonizing scalloped-mediated default repression". Developmental Cell. 25 (4): 388–401. doi:10.1016/j.devcel.2013.04.021. PMC 3705890. PMID 23725764.
  55. ↑ Vassilev A, Kaneko KJ, Shu H, Zhao Y, DePamphilis ML (May 2001). "TEAD/TEF transcription factors utilize the activation domain of YAP65, a Src/Yes-associated protein localized in the cytoplasm". Genes & Development. 15 (10): 1229–41. doi:10.1101/gad.888601. PMC 313800. PMID 11358867.
  56. ↑ Han W, Jung EM, Cho J, Lee JW, Hwang KT, Yang SJ, Kang JJ, Bae JY, Jeon YK, Park IA, Nicolau M, Jeffrey SS, Noh DY (June 2008). "DNA copy number alterations and expression of relevant genes in triple-negative breast cancer". Genes, Chromosomes & Cancer. 47 (6): 490–9. doi:10.1002/gcc.20550. PMID 18314908. Unknown parameter |s2cid= ignored (help)
  57. ↑ Richardson AL, Wang ZC, De Nicolo A, Lu X, Brown M, Miron A, Liao X, Iglehart JD, Livingston DM, Ganesan S (February 2006). "X chromosomal abnormalities in basal-like human breast cancer". Cancer Cell. 9 (2): 121–32. doi:10.1016/j.ccr.2006.01.013. PMID 16473279.
  58. ↑ Nowee ME, Snijders AM, Rockx DA, de Wit RM, Kosma VM, Hämäläinen K, Schouten JP, Verheijen RH, van Diest PJ, Albertson DG, Dorsman JC (September 2007). "DNA profiling of primary serous ovarian and fallopian tube carcinomas with array comparative genomic hybridization and multiplex ligation-dependent probe amplification". The Journal of Pathology. 213 (1): 46–55. doi:10.1002/path.2217. PMID 17668415. Unknown parameter |s2cid= ignored (help)
  59. ↑ Skotheim RI, Autio R, Lind GE, Kraggerud SM, Andrews PW, Monni O, Kallioniemi O, Lothe RA (2006). "Novel genomic aberrations in testicular germ cell tumors by array-CGH, and associated gene expression changes". Cellular Oncology. 28 (5–6): 315–26. doi:10.1155/2006/219786. PMC 4615958. PMID 17167184.
  60. ↑ Landin Malt A, Cagliero J, Legent K, Silber J, Zider A, Flagiello D (2012). "Alteration of TEAD1 expression levels confers apoptotic resistance through the transcriptional up-regulation of Livin". PLOS ONE. 7 (9): e45498. Bibcode:2012PLoSO...745498L. doi:10.1371/journal.pone.0045498. PMC 3454436. PMID 23029054.
  61. ↑ Xia Y, Zhang YL, Yu C, Chang T, Fan HY (2014). "YAP/TEAD co-activator regulated pluripotency and chemoresistance in ovarian cancer initiated cells". PLOS ONE. 9 (11): e109575. Bibcode:2014PLoSO...9j9575X. doi:10.1371/journal.pone.0109575. PMC 4219672. PMID 25369529.
  62. ↑ Yuan H, Liu H, Liu Z, Zhu D, Amos CI, Fang S, Lee JE, Wei Q (August 2015). "Genetic variants in Hippo pathway genes YAP1, TEAD1 and TEAD4 are associated with melanoma-specific survival". International Journal of Cancer. 137 (3): 638–45. doi:10.1002/ijc.29429. PMC 4437894. PMID 25628125.

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