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anti-Human LTBP4 Antibodies:
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Human Polyclonal LTBP4 Primary Antibody for IF (p), IHC (p) - ABIN714626
Choi, de Poot, Lee, Kim, Han, Kim, Finley, Lee: Open-gate mutants of the mammalian proteasome show enhanced ubiquitin-conjugate degradation. in Nature communications 2016
High LTBP4 expression is associated with recurrence in glioblastoma.
Studied the potential role of LTBP-4 in scleroderma through clinical, in vivo and in vitro studies. Results suggest that LTBP-4 protein level is increased in plasma and skin tissue of scleroderma patients; found LTBP-4 to be a potential biomarker to differentiate systemic scleroderma (SSc (show CYP11A1 Antibodies)) from localized scleroderma (LSc (show ARHGEF1 Antibodies)) patients.
The LTBP4 VTTT allele is associated with increased risk of dilated cardiomyopathy in European Americans. LTBP4 protein with the IAAM residues bound more latent TGFbeta (show TGFB1 Antibodies) compared to the LTBP4 VTTT protein.
Our results show that LTBP4 interacts with TGFBR2 (show TGFBR2 Antibodies) and stabilizes TGFbeta (show TGFB1 Antibodies) receptors by preventing their endocytosis and lysosomal degradation in a ligand-dependent and receptor kinase activity-dependent manner.
We show that corticosteroid treatment and the IAAM haplotype of the LTBP4 gene are significantly associated with prolonged ambulation in patients with Duchenne muscular dystrophy (show DMD Antibodies)
In the mdx (show DMD Antibodies) mouse model of Duchenne muscular dystrophy (show DMD Antibodies), the human LTBP4 transgene exacerbated muscular dystrophy symptoms and resulted in weaker muscles with an increased inflammatory infiltrate.
In Caucasians with Duchenne muscular dystrophy (show DMD Antibodies) and LTBP4 genotype there was a protective effect on age at loss of ambulation.
It recruits elastin (show ELN Antibodies) to microfibrils via fibulin-5 (show FBLN5 Antibodies).
LTBP4 haplotype influences age at loss of ambulation, and should be considered in the management of Duchenne muscular dystrophy (show DMD Antibodies) patients.
Latent transforming growth factor beta-binding protein 4 is downregulated in esophageal cancer via promoter methylation.
These data clearly establish a functional link between Ltbp-4L and fibulin-4 (show FBLN4 Antibodies) as a crucial molecular requirement for survival and elastogenesis in mice.
Anxa6 (show ANXA6 Antibodies) and Ltbp4 isoforms modify the extent of damage in acute muscle injury in an additive fashion, and the severe isoform of Ltbp4, characteristic of the DBA (show RPS19 Antibodies)/2J genetic background, correlated with upregulation of Slug and Snail (show SNAI1 Antibodies), and downregulation of Anxa1 (show ANXA1 Antibodies) and Anxa6 (show ANXA6 Antibodies).
Low LTBP4 expression is associated with lung fibrosis.
we found that myostatin (show MSTN Antibodies) forms a complex with LTBP4 and that overexpression of LTBP4 led to a decrease in myostatin (show MSTN Antibodies) levels. LTBP4 also interacted with TGFbeta (show TGFB1 Antibodies) and GDF11 (show GDF11 Antibodies), a protein highly related to myostatin (show MSTN Antibodies). These data identify LTBP4 as a multi-TGFbeta (show TGFB1 Antibodies) family ligand binding protein with the capacity to modify muscle disease through overexpression
Ltbp-4L expression is essential for incorporation of fibulin-4 (show FBLN4 Antibodies) into the extracellular matrix.
These results are consistent with a role for TGFbeta2 in lung septation and for Ltbp4 in regulating fibulin-5 (show FBLN5 Antibodies) dependent elastic fiber assembly.
data suggest a unique function for LTBP-4 during elastic fibrogenesis, making it a potential therapeutic target for elastic fiber regeneration
The lack of LTBP4-mediated targeting in malignant mammary tumor tissues may lead to a possible modification of TGF-ss1 and BMP bioavailability and function.
These data indicate that LTBP-3 and -4 perform partially overlapping functions only in the lungs.
an insertion/deletion polymorphism of 36 bp in the coding region of the Ltbp4 was found in an animal model of muscular dystrophy
The protein encoded by this gene binds transforming growth factor beta (TGFB) as it is secreted and targeted to the extracellular matrix. TGFB is biologically latent after secretion and insertion into the extracellular matrix, and sheds TGFB and other proteins upon activation. Defects in this gene may be a cause of cutis laxa and severe pulmonary, gastrointestinal, and urinary abnormalities. Three transcript variants encoding different isoforms have been found for this gene.
latent transforming growth factor beta binding protein 4
, latent-transforming growth factor beta-binding protein 4-like
, latent transforming growth factor-beta binding protein 4L
, latent-transforming growth factor beta-binding protein 4