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Dorman 601-620 Smart Data Link Module Compatible with Select Ford/Lincoln Models

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Sowden et al. (2001) examined the role of Drosophila 'optomotor blind' (omb)-related T-box genes in the development of human and mouse retina. Murine Tbx2, Tbx3, and Tbx5 and human TBX2 cDNAs were isolated from retina cDNA libraries by hybridization to the Drosophila omb gene. Human and mouse TBX2, TBX3, and TBX5 were expressed asymmetrically across the embryonic neural retina, with highest levels of mRNA within dorsal and peripheral retina. The dorsoventral gradient of TBX2 expression disappeared before the ganglion cell layer (GCL) formed. Its expression became restricted to the inner neuroblastic retina and later to the GCL and inner nuclear layer (INL). The dorsal expression domains of TBX5 and TBX3 were maintained during formation of the GCL. As the retina matured, TBX3 expression was restricted to the INL, and TBX5 was expressed within the GCL. The authors concluded that the expression patterns of TBX2, TBX3, and TBX5 within the developing retina support the idea that the encoded transcription factors play a role in providing positional information important for topographic mapping in differentiation of distinct cell types across the laminar axis of the retina.

In the mouse, 4 of the T-box genes, i.e., the T locus (601397), Tbx1 (602054), Tbx6 (602427), and Tbr1, are dispersed throughout the genome. Li et al. (1997) noted that the other family members, Tbx2 (600747) to Tbx5, exist as 2 clusters, having evolved from a common ancestor by 2 duplication events. Tbx2 and Tbx4 (601719) map together on mouse chromosome 11 (TBX2 is on 17q in the human), and Tbx3 and Tbx5 map on mouse chromosome 5 and human chromosome 12, respectively. However, it is Tbx2 and Tbx3 that form a cognate pair, likewise Tbx4 and Tbx5, with each pair showing related limb-associated expression. A dominant repression domain in Tbx3 mediates transcriptional repression and cell immortalization: relevance to mutations in Tbx3 that cause ulnar-mammary syndrome. Koshiba-Takeuchi, K., Takeuchi, J. K., Arruda, E. P., Kathiriya, I. S., Mo, R., Hui, C., Srivastava, D., Bruneau, B. G.A disabled person is a holder of a valid Blue Badge attending hospital as a patient or visitor or is a disabled person employed by the hospital trust. Disabled patients and visitors receive free parking for the duration of their attendance at, or visit to, the hospital. Disabled employees receive free parking whilst at the hospital for purposes relating to their employment. Basson et al. (1999) showed that TBX5 mutations predicted to create null alleles caused substantial abnormalities in both limb and heart. In contrast, missense mutations of the TBX5 gene produced distinct phenotypes: gly80 to arg ( 601620.0004) caused significant cardiac malformations but only minor skeletal abnormalities, whereas 2 mutations of codon 237, arg237 to gln ( 601620.0003) and arg237 to trp ( 601620.0005), caused extensive upper limb malformations but less significant cardiac abnormalities. They noted that residue 80 is highly conserved within T-box sequences that interact with the major groove of target DNA, whereas residue 237 is located in the T-box domain that selectively binds to the minor groove of DNA. By microdissection of the mouse ventricular conduction system, followed by serial analysis of gene expression (SAGE) of the left bundle branch, Moskowitz et al. (2007) identified Id2 ( 600386) as a conduction system-specific transcript. Analysis of the Id2 promoter showed that conduction system-specific expression of Id2 was dependent on Nkx2.5 and Tbx5. Moskowitz et al. (2007) concluded that a molecular pathway including Id2, Nkx2.5, and Tbx5 coordinates specification of ventricular myocytes into the ventricular conduction system lineage.

Garg et al. (2003) demonstrated that GATA4 (600576) interacts with TBX5 and showed that a missense mutation in GATA4, G296S (600576.0001), abrogated this interaction. Conversely, interaction of GATA4 and TBX5 was disrupted by specific human TBX5 missense mutations that cause similar cardiac septal defects. Garg et al. (2003) concluded that their results implicate GATA4 as a genetic cause of human cardiac septal defects, perhaps through its interaction with TBX5.In affected members of a large 3-generation Turkish family segregating autosomal dominant ulnar-mammary syndrome, Wollnik et al. (2002) identified heterozygosity for a frameshift mutation in TBX3 ( 601621.0004).

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