anti-Scleraxis Homolog A (Mouse) (SCXA) Antikörper

Mouse (Murine) Scleraxis Homolog A (Mouse) (SCXA) Interaktionspartner

1. Deletion of Scx (zeige SCX Antikörper) led to altered long bone properties and callus healing.

2. scleraxis (zeige SCX Antikörper) was required for TGFbeta (zeige TGFB1 Antikörper)-induced fibronectin (zeige FN1 Antikörper) expression: TGFbeta (zeige TGFB1 Antikörper) lost its ability to induce fibronectin (zeige FN1 Antikörper) expression following scleraxis (zeige SCX Antikörper) knockdown.

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

4. Cardiac fibroblast phenotype regulation by scleraxis (zeige SCX Antikörper).

5. scleraxis (zeige SCX Antikörper), 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 (zeige SCX Antikörper) led to impairments in enthesis structure.

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

8. Expression and function of scleraxis (zeige SCX Antikörper) in the developing auditory system.

9. These studies identify an important role for Scx (zeige SCX Antikörper) in regulating proteoglycans in embryonic and mature valve cells.

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

Human Scleraxis Homolog A (Mouse) (SCXA) Interaktionspartner

1. Abnormal upregulation of HIF-2alpha (zeige EPAS1 Antikörper) served as a key switch to direct TSPCs differentiation into osteochondral-lineage rather than teno-lineage. Notably, Scleraxis (Scx (zeige SCX Antikörper)), an essential tendon specific transcription factor, was suppressed on constitutive activation of HIF-2alpha (zeige EPAS1 Antikörper) and mediated the effect of HIF-2alpha (zeige EPAS1 Antikörper) on TSPCs fate decision.

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

3. Scleraxis (zeige SCX Antikörper) 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 (zeige SCX Antikörper) expression.

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

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

7. Scleraxis (zeige SCX Antikörper) thus appears to play a key role in the transcriptional regulation of type I collagen synthesis.