scholarly journals Characterization of follistatin-related gene as a negative regulatory factor for activin family members during mouse heart development

2007 ◽  
Vol 54 (3,4) ◽  
pp. 276-288 ◽  
Author(s):  
Yuka Takehara-Kasamatsu ◽  
Kunihiro Tsuchida ◽  
Masashi Nakatani ◽  
Tatsuya Murakami ◽  
Akira Kurisaki ◽  
...  
Keyword(s):  
Heart Development ◽  
Family Members ◽  
Mouse Heart ◽  
Related Gene ◽  
Regulatory Factor ◽  
Negative Regulatory Factor

scholarly journals Isolation and Characterization of Rat Cytochrome P-450IIB Gene Family Members

1989 ◽  
Vol 264 (12) ◽  
pp. 7046-7053 ◽  
Author(s):  
C M Giachelli ◽  
J Lin-Jones ◽  
C J Omiecinski
Keyword(s):  
Gene Family ◽  
Family Members ◽  
Isolation And Characterization

scholarly journals Genetic and Molecular Characterization of the Maizerp3Rust Resistance Locus

Genetics ◽  
2002 ◽  
Vol 162 (1) ◽  
pp. 381-394 ◽  
Author(s):  
Craig A Webb ◽  
Todd E Richter ◽  
Nicholas C Collins ◽  
Marie Nicolas ◽  
Harold N Trick ◽  
...  
Keyword(s):  
Family Members ◽  
Crossing Over ◽  
Resistance Locus ◽  
Leucine Rich Repeat ◽  
Bac Contig ◽  
Puccinia Sorghi ◽  
Coding Regions ◽  
Complex Locus ◽  
Sequence Identities

AbstractIn maize, the Rp3 gene confers resistance to common rust caused by Puccinia sorghi. Flanking marker analysis of rust-susceptible rp3 variants suggested that most of them arose via unequal crossing over, indicating that rp3 is a complex locus like rp1. The PIC13 probe identifies a nucleotide binding site-leucine-rich repeat (NBS-LRR) gene family that maps to the complex. Rp3 variants show losses of PIC13 family members relative to the resistant parents when probed with PIC13, indicating that the Rp3 gene is a member of this family. Gel blots and sequence analysis suggest that at least 9 family members are at the locus in most Rp3-carrying lines and that at least 5 of these are transcribed in the Rp3-A haplotype. The coding regions of 14 family members, isolated from three different Rp3-carrying haplotypes, had DNA sequence identities from 93 to 99%. Partial sequencing of clones of a BAC contig spanning the rp3 locus in the maize inbred line B73 identified five different PIC13 paralogues in a region of ∼140 kb.

scholarly journals Clinical characterization of 266 patients and family members with cleft lip and/or palate with associated malformations and syndromes

2021 ◽  
Author(s):  
Theodosia Bartzela ◽  
Björn Theuerkauf ◽  
Elisabeth Reichardt ◽  
Malte Spielmann ◽  
Charlotte Opitz
Keyword(s):  
Early Identification ◽  
Congenital Malformations ◽  
Cleft Lip ◽  
Phenotypic Variability ◽  
Family Members ◽  
Pierre Robin Sequence ◽  
Associated Malformations ◽  
Pierre Robin

Abstract Objectives To clinically characterize patients and family members with cleft lip and/or palate (CL/P) and associated congenital malformations or syndromes and propose possible inheritance patterns. Materials and methods An observational study of patients with CL/P, including medical and family history and intra- and extra-oral examination of their family members, was performed. Results Two hundred sixty-six patients, 1257 family members, and 42 pedigrees were included in the study. The distribution of patients according to the cleft type was 57.9% with CLP, 25.2% with cleft palate (CPO), and 12.8% with cleft lip with/without alveolus (CL/A). Seventy-four (27.8%) patients had associated malformations, and 24 (9.2%) a syndrome. The skeletal (27.7%), cardiovascular (19.3%) systems, and eyes (22.9%) were most commonly affected. Pierre Robin Sequence (7 patients) and van der Woude (4) were the most common syndromes. The majority of patients with CPO (19/24) had an associate syndrome. The families had an average of 2.45 affected members. Conclusion Individual and interfamilial phenotypic variability in patients with CL/P makes the understanding of etiopathogenesis challenging. Clinical relevance The overall prevalence of individuals with CL/P and their pedigrees with associated malformations and syndromes emphasize the need for early identification, interdisciplinary, and long-term planning.

Isolation and Characterization of HTLV-I from Symptomatic Family Members with Tropical Spastic Paraparesis (HTLV-I Encephalomyeloneuropathy)

1989 ◽  
Vol 160 (3) ◽  
pp. 371-379 ◽  
Author(s):  
G. McKhann ◽  
C. J. Gibbs ◽  
C. A. Mora ◽  
P. E. Rodgers-Jobnson ◽  
P. P. Liberski ◽  
...  
Keyword(s):  
Family Members ◽  
Spastic Paraparesis ◽  
Tropical Spastic Paraparesis ◽  
Isolation And Characterization

scholarly journals CLONING AND CHARACTERIZATION OF TEMPERATURE-RELATED GENE TRS1

2002 ◽  
Vol 48 (4) ◽  
pp. 273-280 ◽  
Author(s):  
X.-B. Han ◽  
X.-C. Zhou ◽  
Z.-Y. Hu ◽  
Z.-H. Zhang ◽  
Y.-X. Liu
Keyword(s):  
Related Gene

Abstract 124: Function of the Cytoskeletal Proteins Alpha-catenins in Myocardial Growth Control

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Jifen Li ◽  
Sarah Carrante ◽  
Roslyn Yi ◽  
Frans van Roy ◽  
Glenn L. Radice
Keyword(s):  
Heart Development ◽  
Growth Control ◽  
Cytoskeletal Proteins ◽  
Neonatal Rat ◽  
Nuclear Accumulation ◽  
Mouse Heart ◽  
Cardiomyocyte Proliferation ◽  
Rat Cardiomyocytes ◽  
Neonatal Cardiomyocytes

Introduction: Mammalian heart possesses regenerative potential immediately after birth and lost by one week of age. The mechanisms that govern neonatal cardiomyocyte proliferation and regenerative capacity are poorly understood. Recent reports indicate that Yap-Tead transcriptional complex is necessary and sufficient for cardiomyocyte proliferation. During postnatal development, N-cadherin/catenin adhesion complex becomes concentrated at termini of cardiomyocytes facilitating maturation of a specialized intercellular junction structure, the intercalated disc (ICD). This process coincides with the time cardiomyocytes exit cell cycle soon after birth. Hypothesis: We hypothesize that coincident with maturation of ICD α-catenins sequester transcriptional coactivator Yap in cytosol thus preventing activation of genes critical for cardiomyocyte proliferation. Methods: We deleted αE-catenin / αT-catenin genes (α-cat DKO) in perinatal mouse heart and knockdown (KD) α-catenins in neonatal rat cardiomyocytes to study functional impact of α-catenins ablation on ICD maturation. Results: We previously demonstrated that adult α-cat DKO mice exhibited decrease in scar size and improved function post myocardial infarction. In present study, we investigated function of α-catenins during postnatal heart development. We found increase in the number of Yap-positive nuclei (58.7% in DKO vs. 35.8 % in WT, n=13, p<0.001) and PCNA (53.9% in DKO vs. 47.8%, n=8, p<0.05) at postnatal day 1 and day 7 of α-cat DKO heart, respectively. Loss of α-catenins resulted in reduction in N-cadherin at ICD at day 14. We observed an increase number of mononucleated myocytes and decrease number of binucleated myocytes in α-cat DKO compared to controls. Using siRNA KD, we were able to replicate α-cat DKO proliferative phenotype in vitro. The number of BrdU-positive cells was decreased in α-cat KD after interfering with Yap expression (2.91% in α-cat KD vs. 2.02% in α-cat/Yap KD, n>2500 cells, p<0.05), suggesting α-catenins regulate cell proliferation through Yap in neonatal cardiomyocytes. Conclusion: Our results suggest that maturation of ICD regulates α-catenin-Yap interactions in cytosol, thus preventing Yap nuclear accumulation and cardiomyocyte proliferation.

Abstract 255: A Fibroblast Population Shares A Developmental Origin With Cardiovascular Lineages

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Sara Ranjbarvaziri ◽  
Shah Ali ◽  
Mahmood Talkhabi ◽  
Peng Zhao ◽  
Young-Jae Nam ◽  
...  
Keyword(s):  
Heart Development ◽  
Cardiac Fibroblasts ◽  
Immunohistochemical Analysis ◽  
Cell Types ◽  
Mouse Heart ◽  
Developmental Potential ◽  
Reporter Mice ◽  
Significant Difference ◽  
Definition Of

Rationale: The traditional definition of “cardiovascular” lineages describes the eponymous cell types - cardiomyoctes, endothelial cells, and smooth muscle cells - that arise from a common mesodermal progenitor cell during heart development. Fibroblasts are an abundant mesenchymal population in the mammalian heart which may have multiple, discrete developmental origins. Mesp1 represents the earliest marker of cardiovascular progenitors, contributing to the majority of cardiac lineages. To date no link between Mesp1 and fibroblast generation has been reported. Objective: We hypothesized progenitor cells expressing Mesp1 can also give rise to cardiac fibroblasts during heart development. Methods and Results: We generated Mesp1cre/+;R26RmTmG reporter mice where Cre-mediated recombination results in GFP activation in all Mesp1 expressing cells and their progeny. To explore their developmental potential, we isolated GFP+ cells from E7.5 Mesp1cre/+;R26RmTmG mouse. In vitro culture and transplantation studies into SCID mouse kidney capsule as wells as chick embryos showed fibroblastic adoption. Results showed that at E9.5 Mesp1+ and Mesp1- progenitors contributed to the proepicardium organ and later at E11.5 they formed epicardium. Analysis of adult hearts demonstrated that the majority of cardiac fibroblasts are derived from Mesp1 expressing cells. Immunohistochemical analysis of heart sections demonstrated expression of fibroblast markers (including DDR2, PDGFRα and Col1) in cells derived from both Mesp1+ and Mesp1- progenitors. Additionally, we investigated whether the two distinct fibroblast populations have different potency towards reprogramming to cardiomyocytes. Results showed no significant difference between Mesp1 and non-Mesp1 isolated fibroblasts to convert to cardiomyocyte fate. Conclusions: Our data demonstrates that cardiovascular progenitors expressing Mesp1 contribute to the proepicardium. These cells, as cardiovascular progenitors, also give rise to the highest portion of cardiac fibroblasts in the mouse heart.

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