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抗Human LRRC32 抗体:
抗Mouse (Murine) LRRC32 抗体:
抗Rat (Rattus) LRRC32 抗体:
Human Monoclonal LRRC32 Primary Antibody for ELISA, IP - ABIN4230471
Tran, Shevach: Therapeutic potential of FOXP3(+) regulatory T cells and their interactions with dendritic cells. in Human immunology 2009
Show all 3 Pubmed References
Human Monoclonal LRRC32 Primary Antibody for WB - ABIN1981876
Wang, Zhu, Dong, Shi, Lu, Springer: GARP regulates the bioavailability and activation of TGF?. in Molecular biology of the cell 2012
Human Polyclonal LRRC32 Primary Antibody for FACS, WB - ABIN4331580
Macaulay, Thon, Tijssen, Steele, MacDonald, Meade, Burns, Rendon, Salunkhe, Murphy, Bennett, Watkins, He, Fitzgerald, Italiano, Maguire: Canonical Wnt signaling in megakaryocytes regulates proplatelet formation. in Blood 2013
GARP is a surface molecule of regulatory T cells with roles in the regulatory function and TGF-beta releasing [review]
Data show that the Treg activation marker GARP (glycoprotein A repetitions predominant) is expressed on primary melanoma.
High GARP expression is associated with pancreatic cancer and liver metastases from colorectal cancer.
study showed that stimulated, human B lymphocytes produce active TGF-beta1 from surface GARP/latent TGF-beta1 complexes with isotype switching to IgA production.
GARP plays an important role in the pathogenesis of atopic dermatitis.
CD4(+) CD25(+) GARP(+) Treg cells are defective in dilated cardiomyopathy patients and GARP seems to be a better molecular definition of the regulatory phenotype.
these results define the oncogenic effects of the GARP-TGFbeta axis in the tumor microenvironment
LRRC32 expression is significantly upregulated in human masticatory mucosa during wound healing
GARP deficiency leads to accumulation of sphingolipid synthesis intermediates, changes in sterol distribution, and lysosomal dysfunction.
since GARP functions as a transporter of transforming growth factor beta (TGFbeta), a cytokine with broad pleiotropic traits, GARP transcriptional attenuation by alternative promoters might provide a mechanism regulating peripheral TGFb
GARP is regulated by miRNAs and controls latent TGF-beta1 production by human regulatory T cells.
we investigated in detail miR-142-3 pregulation of GARP expression in regulatory CD25(+) CD4 T cells
Findings support the idea that GARP is a new latent TGFbeta-binding protein that regulates the bioavailability of TGFbeta and provides a cell surface platform for alphaV integrin-dependent TGFbeta activation.
There are 2 independent signals, one in C11orf30 and the other in LRRC32, that are strongly associated with serum IgE levels. C11orf30-LRRC32 region may represent a common locus for atopic diseases via pathways involved in regulation of serum IgE levels
GARP is a key receptor controlling FOXP3 in T(reg) cells following T-cell activation in a positive feedback loop assisted by LGALS3 and LGMN
the processing and expression of LRRC32
on chromosome 11q13.5 near the leucine-rich repeat containing 32 gene (LRRC32, also known as GARP) associated with asthma risk
GARP is a regulatory T cell specific cell surface molecule that mediates suppressive signals and induces Foxp3 expression
Platelets and activated Tregs co-express latent TGF-beta and GARP on their membranes.
Expression of GARP on activated regulatory T cells correlates with their suppressive capacity.
Data (including data from studies using knockout mice) suggest that Garp/Lrrc32 is involved in up-regulation of Tgfb3 and is essential for normal embryogenesis of palate; knockout of Garp causes postnatal lethality, cleft palate, and decreased apoptosis and Smad2 phosphorylation in medial edge epithelial cells of palatal shelf of embryos. (Tgfb3 = transforming growth factor beta 3; Smad2 = MAD homolog protein 2)
These results demonstrate the unexpected presence of GARP on Hepatic stellate cells and its significance in regard to the ability of Hepatic stellate cells to activate latent TGF-beta1 and thereby inhibit T cells.
GARP expression on MSCs contributed to their ability to inhibit T-cell responses in vitro.
We conclude that a missense mutation in VPS54, an essential component of the Golgi-associated retrograde protein complex, not only prevents the formation of an acrosome but also initiates a cascade of metabolic abnormalities and a stress reaction.
These findings suggest a role for GARP in natural and induced Treg development through activation of bound latent TGF-beta and signaling, which negatively regulates GARP expression on Tregs.
This gene encodes a type I membrane protein which contains 20 leucine-rich repeats. Alterations in the chromosomal region 11q13-11q14 are involved in several pathologies.
leucine rich repeat containing 32
, leucine-rich repeat-containing protein 32
, leucine-rich repeat-containing protein 32-like
, glycoprotein A repetitions predominant