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Gu, Y.,Gitelman, S. E.,Martincic, D.,Zernik, J. H.,Minkin, C. Korean Academy of Oral Biology and the UCLA Dental 1997 International Journal of Oral Biology Vol.22 No.2
Changes in the expression of alkaline phosphatase (ALP), tartrate-resistant acid phosphatase (TRAP or TrATPase, tartrate-resistant acid-ATPase), and bone morphogenic protein-6 (BMP6, also known as Vgr-1) were characterized during chondrocyte differentiation and osteogenesis in fetal mouse metatarsals. Histochemical observations demonstrate an increase in ALP expression both in differentiating hypertrophic chondrocytes and in osteogenic cells of the surrounding perichondrium/periosteum during days 15, 16, 17, and 18, of gestation. Expression of TRAP is first localized to a few small mononuclear osteoclast precursors in the periosteum of day 16 limbs and then a marked increase is demonstrated between days 17 and 18 of gestation as osteoclasts/chondroclasts invade periosteal bone surfaces and spicules of mineralized cartilage. Enzyme assays show a 9-fold increase in ALP activity in the developing limbs from day 15 to day 18 of gestation (0.05 to 0.43 mmole p-nitrophenol hydrolyzed/min/mg protein), and a 5.5-fold increase in TrATPase activity for the same time period (0.15 to 0.80% [^32P]g-ATP hydrolyzed/min/mg protein). Steady state levels of RNA for ALP, TRAP, and BMP6/Vgr-1 were evaluated using quantitative PCR amplification and our results demonstrate a 5-fold increase in ALP, a 500-fold increase in TRAP/TrATPase, and a 6-fold increase in BMP6/Vgr-1 mRNA levels between days 15 and 18 of gestation.
Four twist genes in zebrafish, four expression patterns
Germanguz, Igal,Lev, Dmitri,Waisman, Tal,Kim, Cheol-Hee,Gitelman, Inna Wiley-Liss, Inc. 2007 Developmental dynamics Vol.236 No.9
<P>Twist genes code for regulatory bHLH proteins essential for embryonic development and conserved across the metazoa. There are four genes that constitute the zebrafish twist family: twist1a, twist1b, twist2, orthologs of the mammalian twist1 and twist2 genes; and twist3—a gene from a new clade that does not exist in mammals. Presented here are their embryonic mRNA expression profiles. The study extends the known conservation of twist developmental patterns in tetrapods to the fish, e.g., expression in cephalic neural crest, sclerotome and lateral plate mesoderm. Some other expression domains are unique, like hypochord and dorsal aorta; some, like the notochord, may be ancestral patterns retained from protochordates; and the expression in invaginating/migrating cells may have been retained from the jellyfish. Perhaps this is one of the more ancient functions of twist—conserved from diploblasts to humans—to facilitate cell movement. Developmental Dynamics 236:2615–2626, 2007. © 2007 Wiley-Liss, Inc.</P>
Identification of new SLE-associated genes with a two-step Bayesian study design
Armstrong, D L,Reiff, A,Myones, B L,Quismorio Jr, F P,Klein-Gitelman, M,McCurdy, D,Wagner-Weiner, L,Silverman, E,Ojwang, J O,Kaufman, K M,Kelly, J A,Merrill, J T,Harley, J B,Bae, S-C,Vyse, T J,Gilkeso Macmillan Publishers Limited 2009 GENES AND IMMUNITY Vol.10 No.5
In our earlier study, we utilized a Bayesian design to probe the association of ∼1000 genes (∼10 000 single-nucleotide polymorphisms (SNPs)) with systemic lupus erythematosus (SLE) on a moderate number of trios of parents and children with SLE. Two genes associated with SLE, with a multitest-corrected false discovery rate (FDR) of <0.05, were identified, and a number of noteworthy genes with FDR of <0.8 were also found, pointing out a future direction for the study. In this report, using a large population of controls and adult- or childhood-onset SLE cases, we have extended the earlier investigation to explore the SLE association of 10 of these noteworthy genes (109 SNPs). We have found that seven of these genes exhibit a significant (FDR<0.05) association with SLE, both confirming some genes that have earlier been found to be associated with SLE (PTPN22 and IRF5) and presenting novel findings of genes (KLRG1, interleukin-16, protein tyrosine phosphatase receptor type T, toll-like receptor (TLR)8 and CASP10), which have not been reported earlier. The results signify that the two-step candidate pathway design is an efficient way to study the genetic foundations of complex diseases. Furthermore, the novel genes identified in this study point to new directions in both the diagnosis and the eventual treatment of this debilitating disease.Genes and Immunity (2009) 10, 446–456; doi:10.1038/gene.2009.38; published online 14 May 2009
Jacob, Chaim O,Zhu, Jiankun,Armstrong, Don L,Yan, Mei,Han, Jie,Zhou, Xin J,Thomas, James A,Reiff, Andreas,Myones, Barry L,Ojwang, Joshua O,Kaufman, Kenneth M,Klein-Gitelman, Marisa,McCurdy, Deborah,Wa National Academy of Sciences 2009 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.106 No.15
<P>A combined forward and reverse genetic approach was undertaken to test the candidacy of IRAK1 (interleukin-1 receptor associated kinase-1) as an X chromosome-encoded risk factor for systemic lupus erythematosus (SLE). In studying approximately 5,000 subjects and healthy controls, 5 SNPs spanning the IRAK1 gene showed disease association (P values reaching 10(-10), odds ratio >1.5) in both adult- and childhood-onset SLE, in 4 different ethnic groups, with a 4 SNP haplotype (GGGG) being strongly associated with the disease. The functional role of IRAK1 was next examined by using congenic mouse models bearing the disease loci: Sle1 or Sle3. IRAK1 deficiency abrogated all lupus-associated phenotypes, including IgM and IgG autoantibodies, lymphocytic activation, and renal disease in both models. In addition, the absence of IRAK1 reversed the dendritic cell 'hyperactivity' associated with Sle3. Collectively, the forward genetic studies in human SLE and the mechanistic studies in mouse models establish IRAK1 as a disease gene in lupus, capable of modulating at least 2 key checkpoints in disease development. This demonstration of an X chromosome gene as a disease susceptibility factor in human SLE raises the possibility that the gender difference in SLE may in part be attributed to sex chromosome genes.</P>