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Journal articles on the topic 'Hand1'

Author: Grafiati

Published: 30 June 2021

Last updated: 2 February 2022

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1

Togi, Kiyonori, Takahiro Kawamoto, Ryoko Yamauchi, Yoshinori Yoshida, Toru Kita, and Makoto Tanaka. "Role of Hand1/eHAND in the Dorso-Ventral Patterning and Interventricular Septum Formation in the Embryonic Heart." Molecular and Cellular Biology 24, no. 11 (June 1, 2004): 4627–35. http://dx.doi.org/10.1128/mcb.24.11.4627-4635.2004.

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ABSTRACT Molecular mechanisms for the dorso-ventral patterning and interventricular septum formation in the embryonic heart are unknown. To investigate a role of Hand1/eHAND in cardiac chamber formation, we generated Hand1/eHAND knock-in mice where Hand1/eHAND cDNA was placed under the control of the MLC2V promoter. In Hand1/eHAND knock-in mice, the outer curvature of the right and left ventricles expanded more markedly. Moreover, there was no interventricular groove or septum formation, although molecularly, Hand1/eHAND knock-in hearts had two ventricles. However, the morphology of the inner curvature of the ventricles, the atrioventricular canal, and the outflow tract was not affected by Hand1/eHAND expression. Furthermore, expression of Hand1/eHAND in the whole ventricles altered the expression patterns of Chisel, ANF, and Hand2/dHAND but did not affect Tbx5 expression. In contrast, the interventricular septum formed normally in transgenic embryos overexpressing Hand1/eHAND in the right ventricle but not in the boundary region. These results suggested that Hand1/eHAND is involved in expansion of the ventricular walls and that absence of Hand1/eHAND expression in the boundary region between the right and left ventricles may be critical in the proper formation of the interventricular groove and septum. Furthermore, Hand1/eHAND is not a master regulatory gene that specifies the left ventricle myocyte lineage but may control the dorso-ventral patterning in concert with additional genes.

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2

Hill, Alison A., and Paul R. Riley. "Differential Regulation of Hand1 Homodimer and Hand1-E12 Heterodimer Activity by the Cofactor FHL2." Molecular and Cellular Biology 24, no. 22 (November 15, 2004): 9835–47. http://dx.doi.org/10.1128/mcb.24.22.9835-9847.2004.

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ABSTRACT The basic helix-loop-helix (bHLH) factor Hand1 plays an essential role in cardiac morphogenesis, and yet its precise function remains unknown. Protein-protein interactions involving Hand1 provide a means of determining how Hand1-induced gene expression in the developing heart might be regulated. Hand1 is known to form either heterodimers with near-ubiquitous E-factors and other lineage-restricted class B bHLH proteins or homodimers with itself in vitro. To date, there have been no reported Hand1 protein interactions involving non-bHLH proteins. Heterodimer-versus-homodimer choice is mediated by the phosphorylation status of Hand1; however, little is known about the in vivo function of these dimers or, importantly, how they are regulated. In an effort to understand how Hand1 activity in the heart might be regulated postdimerization, we have investigated tertiary Hand1-protein interactions with non-bHLH factors. We describe a novel interaction of Hand1 with the LIM domain protein FHL2, a known transcriptional coactivator and corepressor expressed in the developing cardiovascular system. FHL2 interacts with Hand1 via the bHLH domain and is able to repress Hand1/E12 heterodimer-induced transcription but has no effect on Hand1/Hand1 homodimer activity. This effect of FHL2 is not mediated either at the level of dimerization or via an effect of Hand1/E12 DNA binding. In summary, our data describe a novel differential regulation of Hand1 heterodimers versus homodimers by association of the cofactor FHL2 and provide insight into the potential for a tertiary level of control of Hand1 activity in the developing heart.

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3

Firulli, Beth A., Rajani M. George, Jade Harkin, Kevin P. Toolan, Hongyu Gao, Yunlong Liu, Wenjun Zhang, et al. "HAND1 loss-of-function within the embryonic myocardium reveals survivable congenital cardiac defects and adult heart failure." Cardiovascular Research 116, no. 3 (July 9, 2019): 605–18. http://dx.doi.org/10.1093/cvr/cvz182.

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Abstract Aims To examine the role of the basic Helix-loop-Helix (bHLH) transcription factor HAND1 in embryonic and adult myocardium. Methods and results Hand1 is expressed within the cardiomyocytes of the left ventricle (LV) and myocardial cuff between embryonic days (E) 9.5–13.5. Hand gene dosage plays an important role in ventricular morphology and the contribution of Hand1 to congenital heart defects requires further interrogation. Conditional ablation of Hand1 was carried out using either Nkx2.5 knockin Cre (Nkx2.5Cre) or α-myosin heavy chain Cre (αMhc-Cre) driver. Interrogation of transcriptome data via ingenuity pathway analysis reveals several gene regulatory pathways disrupted including translation and cardiac hypertrophy-related pathways. Embryo and adult hearts were subjected to histological, functional, and molecular analyses. Myocardial deletion of Hand1 results in morphological defects that include cardiac conduction system defects, survivable interventricular septal defects, and abnormal LV papillary muscles (PMs). Resulting Hand1 conditional mutants are born at Mendelian frequencies; but the morphological alterations acquired during cardiac development result in, the mice developing diastolic heart failure. Conclusion Collectively, these data reveal that HAND1 contributes to the morphogenic patterning and maturation of cardiomyocytes during embryogenesis and although survivable, indicates a role for Hand1 within the developing conduction system and PM development.

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Firulli, Beth A., Hannah Milliar, Kevin P. Toolan, Jade Harkin, Robyn K. Fuchs, Alex G. Robling, and Anthony B. Firulli. "Defective Hand1 phosphoregulation uncovers essential roles for Hand1 in limb morphogenesis." Development 144, no. 13 (June 2, 2017): 2480–89. http://dx.doi.org/10.1242/dev.149963.

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5

George, Rajani M., and Anthony B. Firulli. "Deletion of a Hand1 lncRNA-Containing Septum Transversum Enhancer Alters lncRNA Expression but Is Not Required for Hand1 Expression." Journal of Cardiovascular Development and Disease 8, no. 5 (May 4, 2021): 50. http://dx.doi.org/10.3390/jcdd8050050.

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We have previously identified a Hand1 transcriptional enhancer that drives expression within the septum transversum, the origin of the cells that contribute to the epicardium. This enhancer directly overlaps a common exon of a predicted family of long non-coding RNAs (lncRNA) that are specific to mice. To interrogate the necessity of this Hand1 enhancer, as well as the importance of these novel lncRNAs, we deleted the enhancer sequences, including the common exon shared by these lncRNAs, using genome editing. Resultant homozygous Hand1 enhancer mutants (Hand1ΔST/ΔST) present with no observable phenotype. Assessment of lncRNA expression reveals that Hand1ΔST/ΔST mutants effectively eliminate detectable lncRNA expression. Expression analysis within Hand1ΔST/ΔST mutant hearts indicates higher levels of Hand1 than in controls. The generation of Hand1 compound heterozygous mutants with the Hand1LacZ null allele (Hand1ΔST/LacZ) also did not reveal any observable phenotypes. Together these data indicate that deletion of this Hand1 enhancer and by consequence a family of murine-specific lncRNAs does not impact embryonic development in observable ways.

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6

Zheng, Mingjie, Shannon Erhardt, Di Ai, and Jun Wang. "Bmp Signaling Regulates Hand1 in a Dose-Dependent Manner during Heart Development." International Journal of Molecular Sciences 22, no. 18 (September 11, 2021): 9835. http://dx.doi.org/10.3390/ijms22189835.

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The bone morphogenetic protein (Bmp) signaling pathway and the basic helix–loop–helix (bHLH) transcription factor Hand1 are known key regulators of cardiac development. In this study, we investigated the Bmp signaling regulation of Hand1 during cardiac outflow tract (OFT) development. In Bmp2 and Bmp4loss-of-function embryos with varying levels of Bmp in the heart, Hand1 is sensitively decreased in response to the dose of Bmp expression. In contrast, Hand1 in the heart is dramatically increased in Bmp4 gain-of-function embryos. We further identified and characterized the Bmp/Smad regulatory elements in Hand1. Combined transfection assays and chromatin immunoprecipitation (ChIP) experiments indicated that Hand1 is directly activated and bound by Smads. In addition, we found that upon the treatment of Bmp2 and Bmp4, P19 cells induced Hand1 expression and favored cardiac differentiation. Together, our data indicated that the Bmp signaling pathway directly regulates Hand1 expression in a dose-dependent manner during heart development.

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7

KNÖFLER, Martin, Gudrun MEINHARDT, Sandra BAUER, Thomas LOREGGER, Richard VASICEK, Debra J. BLOOR, Susan J. KIMBER, and Peter HUSSLEIN. "Human Hand1 basic helix-loop-helix (bHLH) protein: extra-embryonic expression pattern, interaction partners and identification of its transcriptional repressor domains." Biochemical Journal 361, no. 3 (January 25, 2002): 641–51. http://dx.doi.org/10.1042/bj3610641.

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The basic helix-loop-helix (bHLH) transcription factor, Hand1, plays an important role in the development of the murine extra-embryonic trophoblast cell lineage. In the present study, we have analysed the expression of Hand1 in human extra-embryonic cell types and determined its binding specificity and transcriptional activity upon interaction with different class A bHLH factors. Northern blotting and in situ hybridization showed that Hand1 mRNA is specifically expressed in amnion cells at different stages of gestation. Accordingly, we demonstrate that the protein is exclusively produced in the amniotic epithelium in vivo and in purified amnion cells in vitro using a novel polyclonal Hand1 antiserum. Reverse transcriptase-PCR and immunohistochemical staining of blastocysts revealed the production of Hand1 mRNA and polypeptide in the trophectodermal cell layer. In the presence of E12/E47, Hand1 stimulated the transcription of luciferase reporters harbouring degenerate E-boxes, suggesting that E-proteins are potential dimerization partners in trophoblastic tumour and amnion cells. In contrast, Hand1 diminished E12/E47-dependent transcription of reporters containing perfect E-boxes by inhibiting the interaction of Hand1/E-protein heterodimers with the palindromic cognate sequence. Furthermore, we show that Hand1 down-regulated GAL—E12-dependent reporter expression, indicating that the protein can also act directly as a transcriptional repressor. Mutational analyses of GAL-Hand1 suggested that two protein regions located within its N-terminal portion mainly confer the repressing activity. In conclusion, human Hand1 may play an important role in the differentiation of the amniotic membrane and the pre-implanting trophoblast. Furthermore, the data suggest that Hand1 can act as a repressor by two independent mechanisms; sequestration of class A bHLH factors from E-boxes and inhibition of their transcriptional activity.

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8

Asuthkar, Swapna, Maheedhara R. Guda, Sarah E. Martin, Reuben Antony, Karen Fernandez, Julian Lin, Andrew J. Tsung, and Kiran K. Velpula. "Hand1 overexpression inhibits medulloblastoma metastasis." Biochemical and Biophysical Research Communications 477, no. 2 (August 2016): 215–21. http://dx.doi.org/10.1016/j.bbrc.2016.06.045.

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9

Scott, Ian C., Lynn Anson-Cartwright, Paul Riley, Danny Reda, and James C. Cross. "The HAND1 Basic Helix-Loop-Helix Transcription Factor Regulates Trophoblast Differentiation via Multiple Mechanisms." Molecular and Cellular Biology 20, no. 2 (January 15, 2000): 530–41. http://dx.doi.org/10.1128/mcb.20.2.530-541.2000.

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ABSTRACT The basic helix-loop-helix (bHLH) transcription factor genesHand1 and Mash2 are essential for placental development in mice. Hand1 promotes differentiation of trophoblast giant cells, whereas Mash2 is required for the maintenance of giant cell precursors, and its overexpression prevents giant cell differentiation. We found that Hand1 expression and Mash2 expression overlap in the ectoplacental cone and spongiotrophoblast, layers of the placenta that contain the giant cell precursors, indicating that the antagonistic activities ofHand1 and Mash2 must be coordinated. MASH2 and HAND1 both heterodimerize with E factors, bHLH proteins that are the DNA-binding partners for most class B bHLH factors and which are also expressed in the ectoplacental cone and spongiotrophoblast. In vitro, HAND1 could antagonize MASH2 function by competing for E-factor binding. However, the Hand1 mutant phenotype cannot be solely explained by ectopic activity of MASH2, as the Hand1mutant phenotype was not altered by further mutation ofMash2. Interestingly, expression of E-factor genes (ITF2 and ALF1) was down-regulated in the trophoblast lineage prior to giant cell differentiation. Therefore, suppression of MASH2 function, required to allow giant cell differentiation, may occur in vivo by loss of its E-factor partner due to loss of its expression and/or competition from HAND1. In giant cells, where E-factor expression was not detected, HAND1 presumably associates with a different bHLH partner. This may account for the distinct functions of HAND1 in giant cells and their precursors. We conclude that development of the trophoblast lineage is regulated by the interacting functions of HAND1, MASH2, and their cofactors.

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10

Sun, Xiandong, Jian Cao, Haiming Tong, Xizhe Zhang, Yi Sun, Zhimin Wei, and Ronghai Man. "Involvement of HAND1 and CBS in maintenance of cardiac micro-architecture following obesity-induced heart failure." Tropical Journal of Pharmaceutical Research 18, no. 4 (May 18, 2021): 747–52. http://dx.doi.org/10.4314/tjpr.v18i4.10.

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Purpose: To study the role of heart and neural crest derivatives expressed 1 (HAND1) and cystathionine-beta-synthase (CBS) in the maintenance of cardiac architecture following high fat dietinduced obesity. Methods: Mouse models of initial and critical heart disease were established by continuous feeding of high fat diet for 7 and 12 months, respectively. The expression of HAND1 and CBS were assayed using immunohistochemistry and Western blotting. Results: Obesity led to mild and severe forms of heart disease which were confirmed through histological imaging. Initial obesity resulted in cardiac tissue remodeling along with initial degeneration, while critical obesity resulted in tissue hardening. The expression of HAND1 was upregulated 4.3 folds in the mild form of cardiac failure, relative to marginal expression pattern of HAND1 in control tissue. However, as the disease progressed, the expression of HAND1 was limited in serve form of cardiac failure. Moreover, the expression of cystathionine beta-synthase (CBS) was upregulated 3.7-fold in the initial form of heart failure, but was subsequently reduced in serve form of heart disease. Conclusion: These results reveal that in high fat diet-induced cardiac stress, the over-expressions of HAND1 and CBS at the initial stages induce extensive alterations in cardiac architecture.

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11

Awonuga, A. O., M. E. Abdallah, Y. Xie, M. P. Diamond, E. E. Puscheck, and D. Rappolee. "Stress upregulates eomesodermin and HAND1: HAND1 upregulation is stress activated protein kinase-dependent in trophoblast stem cells." Fertility and Sterility 90 (September 2008): S248. http://dx.doi.org/10.1016/j.fertnstert.2008.07.431.

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12

Funato, Noriko, Yuki Taga, Lindsay E. Laurie, Chisa Tometsuka, Masashi Kusubata, and Kiyoko Ogawa-Goto. "The Transcription Factor HAND1 Is Involved in Cortical Bone Mass through the Regulation of Collagen Expression." International Journal of Molecular Sciences 21, no. 22 (November 16, 2020): 8638. http://dx.doi.org/10.3390/ijms21228638.

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Temporal and/or spatial alteration of collagen family gene expression results in bone defects. However, how collagen expression controls bone size remains largely unknown. The basic helix-loop-helix transcription factor HAND1 is expressed in developing long bones and is involved in their morphogenesis. To understand the functional role of HAND1 and collagen in the postnatal development of long bones, we overexpressed Hand1 in the osteochondroprogenitors of model mice and found that the bone volumes of cortical bones decreased in Hand1Tg/+;Twist2-Cre mice. Continuous Hand1 expression downregulated the gene expression of type I, V, and XI collagen in the diaphyses of long bones and was associated with decreased expression of Runx2 and Sp7/Osterix, encoding transcription factors involved in the transactivation of fibril-forming collagen genes. Members of the microRNA-196 family, which target the 3′ untranslated regions of COL1A1 and COL1A2, were significantly upregulated in Hand1Tg/+;Twist2-Cre mice. Mass spectrometry revealed that the expression ratios of alpha 1(XI), alpha 2(XI), and alpha 2(V) in the diaphysis increased during postnatal development in wild-type mice, which was delayed in Hand1Tg/+;Twist2-Cre mice. Our results demonstrate that HAND1 regulates bone size and morphology through osteochondroprogenitors, at least partially by suppressing postnatal expression of collagen fibrils in the cortical bones.

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Gupta, Manoj K., and Tata Rao. "Hearty miR-363 controls HAND1 in cardiac cell specification." Stem Cell Research & Therapy 5, no. 4 (2014): 89. http://dx.doi.org/10.1186/scrt478.

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14

Wang, Juan, Xiao-Qing Hu, Yu-Han Guo, Jian-Yun Gu, Jia-Hong Xu, Yan-Jie Li, Ning Li, Xiao-Xiao Yang, and Yi-Qing Yang. "HAND1 Loss-of-Function Mutation Causes Tetralogy of Fallot." Pediatric Cardiology 38, no. 3 (December 10, 2016): 547–57. http://dx.doi.org/10.1007/s00246-016-1547-8.

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15

Thattaliyath, Bijoy D., Carolina B. Livi, Mark E. Steinhelper, Glenn M. Toney, and Anthony B. Firulli. "HAND1 and HAND2 are expressed in the adult-rodent heart and are modulated during cardiac hypertrophy." Biochemical and Biophysical Research Communications 297, no. 4 (October 2002): 870–75. http://dx.doi.org/10.1016/s0006-291x(02)02297-0.

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16

Vincentz, J. W., N. J. VanDusen, A. B. Fleming, M. Rubart, B. A. Firulli, M. J. Howard, and A. B. Firulli. "A Phox2- and Hand2-Dependent Hand1 cis-Regulatory Element Reveals a Unique Gene Dosage Requirement for Hand2 during Sympathetic Neurogenesis." Journal of Neuroscience 32, no. 6 (February 8, 2012): 2110–20. http://dx.doi.org/10.1523/jneurosci.3584-11.2012.

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17

Risebro, C. A., N. Smart, L. Dupays, R. Breckenridge, T. J. Mohun, and P. R. Riley. "Hand1 regulates cardiomyocyte proliferation versus differentiation in the developing heart." Development 133, no. 22 (October 11, 2006): 4595–606. http://dx.doi.org/10.1242/dev.02625.

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18

Courtney, Jennifer A., Rebecca L. Wilson, James Cnota, and Helen N. Jones. "Conditional Mutation of Hand1 in the Mouse Placenta Disrupts Placental Vascular Development Resulting in Fetal Loss in Both Early and Late Pregnancy." International Journal of Molecular Sciences 22, no. 17 (September 2, 2021): 9532. http://dx.doi.org/10.3390/ijms22179532.

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Congenital heart defects (CHD) affect approximately 1% of all live births, and often require complex surgeries at birth. We have previously demonstrated abnormal placental vascularization in human placentas from fetuses diagnosed with CHD. Hand1 has roles in both heart and placental development and is implicated in CHD development. We utilized two conditionally activated Hand1A126fs/+ murine mutant models to investigate the importance of cell-specific Hand1 on placental development in early (Nkx2-5Cre) and late (Cdh5Cre) pregnancy. Embryonic lethality occurred in Nkx2-5Cre/Hand1A126fs/+ embryos with marked fetal demise occurring after E10.5 due to a failure in placental labyrinth formation and therefore the inability to switch to hemotrophic nutrition or maintain sufficient oxygen transfer to the fetus. Labyrinthine vessels failed to develop appropriately and vessel density was significantly lower by day E12.5. In late pregnancy, the occurrence of Cdh5Cre+;Hand1A126fs/+ fetuses was reduced from 29% at E12.5 to 20% at E18.5 and remaining fetuses exhibited reduced fetal and placental weights, labyrinth vessel density and placenta angiogenic factor mRNA expression. Our results demonstrate for the first time the necessity of Hand1 in both establishment and remodeling of the exchange area beyond early pregnancy and in patterning vascularization of the placental labyrinth crucial for maintaining pregnancy and successful fetal growth.

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19

Hu, Dong, Ian C. Scott, Colleen Geary, Xiang Zhao, and James C. Cross. "The Hand1 transcription factor functions as a homodimer during mouse development." Developmental Biology 295, no. 1 (July 2006): 369. http://dx.doi.org/10.1016/j.ydbio.2006.04.134.

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20

Courtney, Jennifer, and Helen Jones. "Late-gestation fetal demise in endothelial-specific Hand1 dominant-negative mice." Placenta 83 (August 2019): e69. http://dx.doi.org/10.1016/j.placenta.2019.06.223.

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21

Morikawa, Y. "Extra-embryonic vasculature development is regulated by the transcription factor HAND1." Development 131, no. 9 (March 31, 2004): 2195–204. http://dx.doi.org/10.1242/dev.01091.

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22

Cheng, Zhi, Lin Lib, Zhongzhi Li, Mugen Liu, Jinting Yan, Binbin Wang, and Xu Ma. "Two novel HAND1 mutations in Chinese patients with ventricular septal defect." Clinica Chimica Acta 413, no. 7-8 (April 2012): 675–77. http://dx.doi.org/10.1016/j.cca.2011.10.014.

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23

Okubo, Chikako, Megumi Narita, Azusa Inagaki, Misato Nishikawa, Akitsu Hotta, Shinya Yamanaka, and Yoshinori Yoshida. "Expression dynamics of HAND1/2 in in vitro human cardiomyocyte differentiation." Stem Cell Reports 16, no. 8 (August 2021): 1906–22. http://dx.doi.org/10.1016/j.stemcr.2021.06.014.

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24

McFadden, D. G. "The Hand1 and Hand2 transcription factors regulate expansion of the embryonic cardiac ventricles in a gene dosage-dependent manner." Development 132, no. 1 (December 2, 2004): 189–201. http://dx.doi.org/10.1242/dev.01562.

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25

Xu, Wen. "Expression Data Analysis to Identify Biomarkers Associated with Asthma in Children." International Journal of Genomics 2014 (2014): 1–5. http://dx.doi.org/10.1155/2014/165175.

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Asthma is characterized by recurrent episodes of wheezing, shortness of breath, chest tightness, and coughing. It is usually caused by a combination of complex and incompletely understood environmental and genetic interactions. We obtained gene expression data with high-throughput screening and identified biomarkers of children's asthma using bioinformatics tools. Next, we explained the pathogenesis of children's asthma from the perspective of gene regulatory networks: DAVID was applied to perform Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enriching analysis for the top 3000 pairs of relationships in differentially regulatory network. Finally, we found that HAND1, PTK1, NFKB1, ZIC3, STAT6, E2F1, PELP1, USF2, and CBFB may play important roles in children's asthma initiation. On account of regulatory impact factor (RIF) score, HAND1, PTK7, and ZIC3 were the potential asthma-related factors. Our study provided some foundations of a strategy for biomarker discovery despite a poor understanding of the mechanisms underlying children's asthma.

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Li, Li, Juan Wang, Xing-Yuan Liu, Hua Liu, Hong-Yu Shi, Xiao-Xiao Yang, Ning Li, et al. "HAND1 loss-of-function mutation contributes to congenital double outlet right ventricle." International Journal of Molecular Medicine 39, no. 3 (January 20, 2017): 711–18. http://dx.doi.org/10.3892/ijmm.2017.2865.

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BRECKENRIDGE, R., Z. ZUBERI, L. FELKIN, E. BIRKS, P. BARTON, A. TINKER, and T. MOHUN. "Overexpression of the transcription factor Hand1 causes sudden cardiac death in mice." European Journal of Heart Failure Supplements 7 (June 2008): 109. http://dx.doi.org/10.1016/s1567-4215(08)60301-x.

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Breckenridge, Ross A., Zia Zuberi, John Gomes, Robert Orford, Laurent Dupays, Leanne E. Felkin, James E. Clark, et al. "Overexpression of the transcription factor Hand1 causes predisposition towards arrhythmia in mice." Journal of Molecular and Cellular Cardiology 47, no. 1 (July 2009): 133–41. http://dx.doi.org/10.1016/j.yjmcc.2009.04.007.

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Laurie, Lindsay E., Hiroki Kokubo, Masataka Nakamura, Yumiko Saga, and Noriko Funato. "The Transcription Factor Hand1 Is Involved In Runx2-Ihh-Regulated Endochondral Ossification." PLOS ONE 11, no. 2 (February 26, 2016): e0150263. http://dx.doi.org/10.1371/journal.pone.0150263.

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30

Yamada, Kayo, Hiromi Kanda, Satoshi Tanaka, Nobuhiko Takamatsu, Tadayoshi Shiba, and Michihiko Ito. "Sox15 enhances trophoblast giant cell differentiation induced by Hand1 in mouse placenta." Differentiation 74, no. 5 (June 2006): 212–21. http://dx.doi.org/10.1111/j.1432-0436.2006.00070.x.

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31

Riley, Pual, Lynn Anaon-Cartwight, and James C. Cross. "The Hand1 bHLH transcription factor is essential for placentation and cardiac morphogenesis." Nature Genetics 18, no. 3 (March 1998): 271–75. http://dx.doi.org/10.1038/ng0398-271.

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32

Breckenridge, Ross A., Izabela Piotrowska, Keat-Eng Ng, Timothy J. Ragan, James A. West, Surendra Kotecha, Norma Towers, et al. "Hypoxic Regulation of Hand1 Controls the Fetal-Neonatal Switch in Cardiac Metabolism." PLoS Biology 11, no. 9 (September 24, 2013): e1001666. http://dx.doi.org/10.1371/journal.pbio.1001666.

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33

Breckenridge, R. A., M. T. Neary, M. Bennett, S. Kotecha, J. Griffin, and T. J. Mohun. "18 Hypoxia-driven Hand1 expression controls changes in cardiac metabolism around birth." Heart 97, no. 24 (November 24, 2011): e8-e8. http://dx.doi.org/10.1136/heartjnl-2011-301156.18.

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Arnold, Daniel R., Vilceu Bordignon, Réjean Lefebvre, Bruce D. Murphy, and Lawrence C. Smith. "Somatic cell nuclear transfer alters peri-implantation trophoblast differentiation in bovine embryos." Reproduction 132, no. 2 (August 2006): 279–90. http://dx.doi.org/10.1530/rep.1.01217.

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Abnormal placental development limits success in ruminant pregnancies derived from somatic cell nuclear transfer (SCNT), due to reduction in placentome number and consequently, maternal/fetal exchange. In the primary stages of an epithelial–chorial association, the maternal/fetal interface is characterized by progressive endometrial invasion by specialized trophoblast binucleate/giant cells (TGC). We hypothesized that dysfunctional placentation in SCNT pregnancies results from aberration in expression of genes known to be necessary for trophoblast proliferation (Mash2), differentiation (Hand1), and function (IFN-τ and PAG-9). We, therefore, compared the expression of these factors in trophoblast from bovine embryos derived from artificial insemination (AI), in vitro fertilization (IVF), and SCNT prior to (day 17) and following (day 40 of gestation) implantation, as well as TGC densities and function. In preimplantation embryos, Mash2 mRNA was more abundant in SCNT embryos compared to AI, while Hand1 was highest in AI and IVF relative to SCNT embryos. IFN-τ mRNA abundance did not differ among groups. PAG-9 mRNA was undetectable in SCNT embryos, present in IVF embryos and highest in AI embryos. In postimplantation pregnancies, SCNT fetal cotyledons displayed higher Mash2 and Hand1 than AI and IVF tissues. Allelic expression of Mash2 was not different among the groups, which suggests that elevated mRNA expression was not due to altered imprinting status of Mash2. The day 40 SCNT cotyledons had the fewest number of TGC compared to IVF and AI controls. Thus, expression of genes critical to normal placental development is altered in SCNT bovine embryos, and this is expected to cause abnormal trophoblast differentiation and contribute to pregnancy loss.

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Firulli, Beth A., David P. McConville, James S. Byers III, Joshua W. Vincentz, Ralston M. Barnes, and Anthony B. Firulli. "Analysis of a Hand1 hypomorphic allele reveals a critical threshold for embryonic viability." Developmental Dynamics 239, no. 10 (August 24, 2010): 2748–60. http://dx.doi.org/10.1002/dvdy.22402.

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36

Granger, Darla K., Warren C. Briedenbach, Diane J. Pidwell, Jon W. Jones, Lee Ann Baxter-Lowe, and Christina L. Kaufman. "Lack of donor hyporesponsiveness and donor chimerism after clinical transplantation of the hand1." Transplantation 74, no. 11 (December 2002): 1624–30. http://dx.doi.org/10.1097/00007890-200212150-00022.

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Firulli, B. A., R. K. Fuchs, J. W. Vincentz, D. E. Clouthier, and A. B. Firulli. "Hand1 phosphoregulation within the distal arch neural crest is essential for craniofacial morphogenesis." Development 141, no. 15 (July 22, 2014): 3050–61. http://dx.doi.org/10.1242/dev.107680.

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Martindill, David M. J., Catherine A. Risebro, Nicola Smart, Maria Del Mar Franco-Viseras, Carla O. Rosario, Carol J. Swallow, James W. Dennis, and Paul R. Riley. "Nucleolar release of Hand1 acts as a molecular switch to determine cell fate." Nature Cell Biology 9, no. 10 (September 23, 2007): 1131–41. http://dx.doi.org/10.1038/ncb1633.

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Abdallah, M., Y. Xie, E. E. Puscheck, D. A. Rappolee, and A. O. Awonuga. "Benzopyrene activates SAPK and induces HAND1 that favors differentiation of trophoblast stem cells." Fertility and Sterility 92, no. 3 (September 2009): S136—S137. http://dx.doi.org/10.1016/j.fertnstert.2009.07.1208.

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Byl, Nancy, Debra Hamati, Marsha Melnick, Frank Wilson, and Alison McKenzie. "The sensory consequences of repetitive strain injury in musicians: focal dystonia of the hand1." Journal of Back and Musculoskeletal Rehabilitation 7, no. 1 (July 1, 1996): 27–39. http://dx.doi.org/10.3233/bmr-1996-7105.

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Pearton, David J., Craig S. Smith, Emma Redgate, Jessica van Leeuwen, Martyn Donnison, and Peter L. Pfeffer. "Elf5 counteracts precocious trophoblast differentiation by maintaining Sox2 and 3 and inhibiting Hand1 expression." Developmental Biology 392, no. 2 (August 2014): 344–57. http://dx.doi.org/10.1016/j.ydbio.2014.05.012.

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Hu, Dong, Ian C. Scott, Fran Snider, Colleen Geary-Joo, Xiang Zhao, David G. Simmons, and James C. Cross. "The basic helix-loop-helix transcription factor Hand1 regulates mouse development as a homodimer." Developmental Biology 382, no. 2 (October 2013): 470–81. http://dx.doi.org/10.1016/j.ydbio.2013.07.025.

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Firulli, Beth A., Kevin P. Toolan, Jade Harkin, Hannah Millar, Santiago Pineda, and Anthony B. Firulli. "The HAND1 frameshift A126FS mutation does not cause hypoplastic left heart syndrome in mice." Cardiovascular Research 113, no. 14 (August 31, 2017): 1732–42. http://dx.doi.org/10.1093/cvr/cvx166.

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Reamon-Buettner, Stella Marie, Yari Ciribilli, Ilaria Traverso, Beate Kuhls, Alberto Inga, and Juergen Borlak. "A functional genetic study identifies HAND1 mutations in septation defects of the human heart." Human Molecular Genetics 18, no. 19 (July 7, 2009): 3567–78. http://dx.doi.org/10.1093/hmg/ddp305.

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Lu, Shuangshuang, Pan Du, Congjia Shan, Yaohe Wang, Changsheng Ma, and Jianzeng Dong. "Haploinsufficiency of Hand1 improves mice survival after acute myocardial infarction through preventing cardiac rupture." Biochemical and Biophysical Research Communications 478, no. 4 (September 2016): 1726–31. http://dx.doi.org/10.1016/j.bbrc.2016.09.012.

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Coz, Florian Le, Noriyuki Suzuki, Hirohisa Nagahori, Takashi Omori, and Koichi Saito. "Hand1-Luc Embryonic Stem Cell Test (Hand1-Luc EST): A novel rapid and highly reproducible in vitro test for embryotoxicity by measuring cytotoxicity and differentiation toxicity using engineered mouse ES cells." Journal of Toxicological Sciences 40, no. 2 (2015): 251–61. http://dx.doi.org/10.2131/jts.40.251.

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Smart, Nicola, Alison A. Hill, James C. Cross, and Paul R. Riley. "A differential screen for putative targets of the bHLH transcription factor Hand1 in cardiac morphogenesis." Mechanisms of Development 119 (December 2002): S65—S71. http://dx.doi.org/10.1016/s0925-4773(03)00093-5.

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Morin, Steves, Gina Pozzulo, Lynda Robitaille, Jay Cross, and Mona Nemer. "MEF2-dependent Recruitment of the HAND1 Transcription Factor Results in Synergistic Activation of Target Promoters." Journal of Biological Chemistry 280, no. 37 (July 25, 2005): 32272–78. http://dx.doi.org/10.1074/jbc.m507640200.

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Wang, Jian, Yanan Lu, Huiwen Chen, Minzhi Yin, Tingting Yu, and Qihua Fu. "Investigation of somatic NKX2-5, GATA4 and HAND1 mutations in patients with tetralogy of Fallot." Pathology 43, no. 4 (June 2011): 322–26. http://dx.doi.org/10.1097/pat.0b013e32834635a9.

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Åblad, B., G. Johnsson, and M. Henning. "The Effect of Intra-arterially Administrated Hydralazine on Blood Flow in the Forearm and Hand1)." Acta Pharmacologica et Toxicologica 18, no. 3 (March 13, 2009): 191–98. http://dx.doi.org/10.1111/j.1600-0773.1961.tb00331.x.

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