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TBX4 is a member of a phylogenetically conserved family of genes that share a common DNA-binding domain, the T-box. Additionally we are shipping TBX4 Proteins (3) and and many more products for this protein.
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We propose phenotypic expansion of the TBX4-related clinical disease spectrum to include acinar dysplasia of the lungs. The reported mutation is the first identified genetic variant causative for acinar dysplasia.
TBX4 is a mesenchymal transcription factor that drives accumulation of myofibroblasts and the development of lung fibrosis
In a cohort with idiopathic or hereditary pulmonary arterial hypertension, a possibly associated mutation was found in 11.10% of the idiopathic cases (n = 16) and in 68.18% of the hereditary cases. There were 4 mutations found in TBX4.
a low level of TBX4 expression suggests a worse prognosis for patients with stage II PDAC. Down-regulation of the TBX4 gene in pancreas is less likely to be regulated by DNA methylation (show HELLS Antibodies).
Although TBX4 remains the candidate gene for congenital clubfoot involving 17q23.1-q23.2 duplications, the explanation for variable expressivity and penetrance remains unknown.
data indicate that TBX4 mutations are associated with childhood-onset pulmonary arterial hypertension (PAH), but the prevalence of PAH in adult TBX4 mutation carriers is low
Minimal evidence was found for an association between TBX4 and clubfoot and no pathogenic sequence variants were identified in the two known TBX4 hindlimb enhancer elements.
Microdeletion of 17q22q23.2 encompassing TBX2 (show TBX2 Antibodies) and TBX4 in a patient with congenital microcephaly, thyroid duct cyst, sensorineural hearing loss, and pulmonary hypertension.
Mutations in the human TBX4 gene cause small patella syndrome
These data extend our understanding of the role and regulation of Tbx4 and Shox2 (show SHOX2 Antibodies) in limb development and limb associated diseases.
Although postnatal deletion of Tbx4 in oocytes does not obviously impair fertility, it is possible that the reduction in primordial germ cells observed in Tbx4 homozygous null mutant embryos could affect long-term fertility in adults.
Candidate gene approach identifies multiple genes and signaling pathways downstream of Tbx4 in the developing allantois
Mice deficient in Tbx4 and Tbx5 (show TBX5 Antibodies) show severely reduced lung branching at mid-gestation.
Tbx4 expression and lineage reveal that various distinct appendages, such as the allantois, hindlimb, and external genitalia, all arise from a single mesenchymal expression domain.
It was shown that, firstly, Pitx1 (show PITX1 Antibodies) influences hindlimb outgrowth by regulating Tbx4 expression levels and that, subsequently,Pitx1 (show PITX1 Antibodies) shapes hindlimb bone and soft tissue morphology independently of Tbx4.
Study find that Tbx4 is the primary effector of HL identity for both skeletal and muscle development.
Tbx4 is reported to play a key role in separation of the respiratory tract and the esophagus.
Deletion of Tbx4 in hindlimbs specifically affects muscle and tendon patterning without disrupting skeletal development, thus suggesting that distinct cues regulate these processes.
This gene is a member of a phylogenetically conserved family of genes that share a common DNA-binding domain, the T-box. T-box genes encode transcription factors involved in the regulation of developmental processes. This gene is the human homolog of mouse Tbx4, which is closely linked to Tbx2 on mouse chromosome 11. Similarly this gene, like TBX2, maps to human chromosome 17. Expression studies in mouse and chicken show that Tbx4 is expressed in developing hindlimb, but not in forelimb buds, suggesting a role for this gene in regulating limb development and specification of limb identity.
T-box gene 4
, T-box transcription factor TBX4
, T-Box protein 4
, T-box 4
, T-box transcription factor TBX4-like
, t-box transcription factor TBX4-like
, T-box 4 protein
, T-box protein 4
, transcription factor Tbx4