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anti-Mouse (Murine) Antibodies:
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Human Polyclonal SH3PXD2B Primary Antibody for IHC, IHC (p) - ABIN4353279
Wilson, Sunley, Smith, Pope, Bromhead, Fitzpatrick, Di Rocco, van Steensel, Coman, Leventer, Delatycki, Amor, Bahlo, Lockhart: Mutations in SH3PXD2B cause Borrone dermato-cardio-skeletal syndrome. in European journal of human genetics : EJHG 2014
The interaction of Tks4 with Src may result in the long term stabilization of the kinase in its active conformation, leading to prolonged Src activity following epidermal growth factor stimulation.
We report a sibling pair with Frank-ter Haar syndrome (FTHS) caused by a homozygous, novel mutation pLys133Glnfs*13 in the SH3PXD2B gene.
Suggest the importance of Tks adaptor proteins in melanoma growth and metastasis in vivo is likely via functional invadopodia formation.
Misfolded Frank-ter Haar syndrome protein Tks4(R43W) is transported via the microtubule system to the aggresomes.
a new function for Tks4 in the regulation of growth factor-dependent cell migration.
SH3PXD2B is a scaffold protein that plays a key role in regulating the actin cytoskeleton via Src and cortactin.
Tks4 and Tks5 directly bind to NoxA1. The integrity of the N-terminal PRR of NoxA1 is essential for this direct interaction with the Tks proteins.
The Nox1-dependent generation of reactive oxygen species is dependent on Src phosphorylation of NoxA1 and Tks4. Blockage of phosphorylation of NoxA1 and Tks4 decreases Nox1-dependent ROS generation and blocks SrcYF-induced invadopodia formation.
These findings establish a role for TKS4 in Frank-Ter Haar syndrome and embryonic development.
together, these results establish a novel function for Tks4 in the regulation of mesenchymal stromal cells differentiation.
eyes of B10-Sh3pxd2bnee mice exhibit multiple features of congenital glaucoma.
The mouse model with a mutation in the Sh3pxd2b gene (Sh3pxd2b(nee)) mirrors craniofacial dysmorphology and otitis media in humans.
SH3PXD2B is a podosomal-adaptor protein required for postnatal growth and development.
Induction of the fad49 gene was observed in adipocyte differentiable 3T3-L1 cells, but not in non-adipogenic NIH-3T3 cells.
Tks4 has a role in the formation and function of podosomes.
Silencing of C/EBPdelta impaired the expression of factor for adipocyte differentiation (fad) 49, which is up-regulated and plays a crucial role early in adipogenesis.
This gene encodes an adapter protein that is characterized by a PX domain and four Src homology 3 domains. The encoded protein is required for podosome formation and is involved in cell adhesion and migration of numerous cell types. Mutations in this gene are the cause of Frank-ter Haar syndrome.
SH3 and PX domain-containing protein 2B
, adapter protein HOFI
, adaptor protein HOFI
, factor for adipocyte differentiation 49
, tyrosine kinase substrate with four SH3 domains