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anti-Human LTBP4 Antikörper:
anti-Mouse (Murine) LTBP4 Antikörper:
anti-Rat (Rattus) LTBP4 Antikörper:
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Human Polyclonal LTBP4 Primary Antibody für 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 (zeige CYP11A1 Antikörper)) from localized scleroderma (LSc (zeige ARHGEF1 Antikörper)) 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 (zeige TGFB1 Antikörper) compared to the LTBP4 VTTT protein.
Our results show that LTBP4 interacts with TGFBR2 (zeige TGFBR2 Antikörper) and stabilizes TGFbeta (zeige TGFB1 Antikörper) 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 (zeige DMD Antikörper)
In the mdx (zeige DMD Antikörper) mouse model of Duchenne muscular dystrophy (zeige DMD Antikörper), the human LTBP4 transgene exacerbated muscular dystrophy symptoms and resulted in weaker muscles with an increased inflammatory infiltrate.
In Caucasians with Duchenne muscular dystrophy (zeige DMD Antikörper) and LTBP4 genotype there was a protective effect on age at loss of ambulation.
It recruits elastin (zeige ELN Antikörper) to microfibrils via fibulin-5 (zeige FBLN5 Antikörper).
LTBP4 haplotype influences age at loss of ambulation, and should be considered in the management of Duchenne muscular dystrophy (zeige DMD Antikörper) patients.
Latent transforming growth factor beta-binding protein 4 is downregulated in esophageal cancer via promoter methylation.
Low LTBP4 expression is associated with lung fibrosis.
we found that myostatin (zeige MSTN Antikörper) forms a complex with LTBP4 and that overexpression of LTBP4 led to a decrease in myostatin (zeige MSTN Antikörper) levels. LTBP4 also interacted with TGFbeta (zeige TGFB1 Antikörper) and GDF11 (zeige GDF11 Antikörper), a protein highly related to myostatin (zeige MSTN Antikörper). These data identify LTBP4 as a multi-TGFbeta (zeige TGFB1 Antikörper) family ligand binding protein with the capacity to modify muscle disease through overexpression
Ltbp-4L expression is essential for incorporation of fibulin-4 (zeige FBLN4 Antikörper) into the extracellular matrix.
These results are consistent with a role for TGFbeta2 in lung septation and for Ltbp4 in regulating fibulin-5 (zeige FBLN5 Antikörper) 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
LTBP-4 has a role in targeting and activation of TGF-beta1 (zeige TGFB1 Antikörper) which regulates BMP-4 (zeige BMP4 Antikörper) 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 (zeige TGFB1 Antikörper) 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