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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
DMD gene mutations involving the hinge 3 region, actin-binding domain, and exons 45-49, as well as the LTBP4 IAAM haplotype, were not associated with age of left ventricular dysfunction onset inDuchenne muscular dystrophy.
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) from localized scleroderma (LSc) 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 compared to the LTBP4 VTTT protein.
Our results show that LTBP4 interacts with TGFBR2 and stabilizes TGFbeta 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
In the mdx mouse model of Duchenne muscular dystrophy, the human LTBP4 transgene exacerbated muscular dystrophy symptoms and resulted in weaker muscles with an increased inflammatory infiltrate.
In Caucasians with Duchenne muscular dystrophy and LTBP4 genotype there was a protective effect on age at loss of ambulation.
It recruits elastin to microfibrils via fibulin-5.
LTBP4 haplotype influences age at loss of ambulation, and should be considered in the management of Duchenne muscular dystrophy patients.
Latent transforming growth factor beta-binding protein 4 is downregulated in esophageal cancer via promoter methylation.
Data indicate mutations of FBLN4, FBLN5, and LTBP4 in 12 probands presenting with type 1 recessive cutis laxa.
the G1 and G3 domains of versican were upregulated and LTBP-4 was downregulated in breast cancer stroma
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.
Meta-analysis of abdominal aortic aneurysm size and growth rates demonstrated a significant association with the LTBP4 21011A>T genotype (a 2% decrease in AAA diameter, or a 0.53 mm/year reduction in AAA growth rate, per T allele [p=0.03, p=0.01]).
These data suggest that LTBP-4 functions are modified by tissue-specific expression of the two N-terminally distinct variants, which in addition exhibit significant differences in cellular processing and targeting.
Extracellular matrix is an important site of deposition for LTBP-3 and LTBP-4.
Our findings suggest that variations in or near the HPN and LTBP4 genes do not play a role in the susceptibility to IA in the Dutch population.
Novel functions for LTBP-4 as an adhesion molecule.
Mutations in LTBP4 cause a syndrome of impaired pulmonary, gastrointestinal, genitourinary, musculoskeletal, and dermal development.
These data suggest that LTBP-2 and -4 have critical overlapping functions in forming the robust structure of microfibrils in vitro and in vivo.
Ltbp4 regulates Pdgfrb expression via TGFbeta-dependent modulation of Nrf2 transcription factor function.
These data clearly establish a functional link between Ltbp-4L and fibulin-4 as a crucial molecular requirement for survival and elastogenesis in mice.
Anxa6 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/2J genetic background, correlated with upregulation of Slug and Snail, and downregulation of Anxa1 and Anxa6.
Low LTBP4 expression is associated with lung fibrosis.
we found that myostatin forms a complex with LTBP4 and that overexpression of LTBP4 led to a decrease in myostatin levels. LTBP4 also interacted with TGFbeta and GDF11, a protein highly related to myostatin. These data identify LTBP4 as a multi-TGFbeta family ligand binding protein with the capacity to modify muscle disease through overexpression
Ltbp-4L expression is essential for incorporation of fibulin-4 into the extracellular matrix.
These results are consistent with a role for TGFbeta2 in lung septation and for Ltbp4 in regulating fibulin-5 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
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
Mice homozygous for the disrupted allele develop severe pulmonary emphysema, cardiomyopathy, and colorectal cancer.
LTBP-4 has a role in targeting and activation of TGF-beta1 which regulates BMP-4 signaling in mouse lung
Results indicate taht there are two separate functions of LTBP-4, as a regulator of elastic fiber assembly and of TGF-beta levels in lungs.
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