Scleraxis Homolog A (Mouse) Proteins (SCXA)

Mouse (Murine) Scleraxis Homolog A (Mouse) (SCXA) interaction partners

1. Deletion of Scx led to altered long bone properties and callus healing.

2. scleraxis was required for TGFbeta-induced fibronectin expression: TGFbeta lost its ability to induce fibronectin expression following scleraxis knockdown.

3. The phosphorylation sequence matched that targeted by Casein Kinase 2, and inhibition of this kinase activity disrupted the ability of scleraxis to modulate the expression of its target genes while also attenuating TGFbeta (show TGFB1 Proteins)-induced expression of type I collagen and myofibroblast phenotype conversion marker genes

4. Cardiac fibroblast phenotype regulation by scleraxis.

5. scleraxis, a transcription factor critically involved in embryonic tendon development and formation, plays a pivotal role in the fate determination of mesenchymal stem cells towards tenocyte differentiation.

6. deletion of Scx led to impairments in enthesis structure.

7. several mRNAs are affected by alternative splicing events in the absence of Scx, suggesting additional roles in post-transcriptional modification.

8. Expression and function of scleraxis in the developing auditory system.

9. These studies identify an important role for Scx in regulating proteoglycans in embryonic and mature valve cells.

10. paratenon cells, which normally do not express Scx, respond to injury by turning on Scx and assembling matrix to bridge the defect

Human Scleraxis Homolog A (Mouse) (SCXA) interaction partners

1. Abnormal upregulation of HIF-2alpha served as a key switch to direct TSPCs differentiation into osteochondral-lineage rather than teno-lineage. Notably, Scleraxis (Scx), an essential tendon specific transcription factor, was suppressed on constitutive activation of HIF-2alpha and mediated the effect of HIF-2alpha on TSPCs fate decision.

2. These studies identify an important role for Scx in regulating proteoglycans in embryonic and mature valve cells.

3. Scleraxis was expressed in periodontal ligament cells, bone marrow cells, and gingival fibroblasts, and may play an important role in differentiation of periodontal ligament cells.

4. High glucose inhibited osteogenetic differentiation of periodontal ligament cells and up-regulated Scleraxis expression.

5. Scx and E47 (show TCF3 Proteins) might modulate the primary chondrogenesis by associating with the Sox9 (show SOX9 Proteins)-related transcriptional complex, and by binding to the conserved E-box on Col2a1 (show COL2A1 Proteins) promoter.

6. collagen type I and several T/L-related proteoglycans were upregulated in hMSC-Scx cells

7. Scleraxis thus appears to play a key role in the transcriptional regulation of type I collagen synthesis.