Browse our anti-LRRC32 (LRRC32) Antibodies

Human Leucine Rich Repeat Containing 32 (LRRC32) interaction partners

1. This review summarizes the most important features of GARP biology described to date including gene regulation, protein expression and mechanism in activating latent TGF-beta, and the function of GARP in regulatory T cell biology and peripheral tolerance, as well as GARP's increasingly recognized roles in platelet-mediated cancer immune evasion. [review]

2. Increased GARP expression in papillary thyroid cancer was positively correlated with increased expression of Foxp3, which is very important for development of Tregs. But, there is no significant association of elevated expression of GARP with lymph node metastasis in papillary thyroid cancer.

3. This finding reveals how GARP exploits an unusual medley of interactions, including fold complementation by the amino terminus of TGF-beta1, to chaperone and orient the cytokine for binding and activation by alphaVbeta8.

4. GARP is a surface molecule of regulatory T cells with roles in the regulatory function and TGF-beta releasing [review]

5. Data show that the Treg activation marker GARP (glycoprotein A repetitions predominant) is expressed on primary melanoma.

6. High GARP expression is associated with pancreatic cancer and liver metastases from colorectal cancer.

7. study showed that stimulated, human B lymphocytes produce active TGF-beta1 from surface GARP/latent TGF-beta1 complexes with isotype switching to IgA production.

8. GARP plays an important role in the pathogenesis of atopic dermatitis.

9. CD4(+) CD25(+) GARP(+) Treg cells are defective in dilated cardiomyopathy patients and GARP seems to be a better molecular definition of the regulatory phenotype.

10. these results define the oncogenic effects of the GARP-TGFbeta axis in the tumor microenvironment

11. LRRC32 expression is significantly upregulated in human masticatory mucosa during wound healing

12. GARP deficiency leads to accumulation of sphingolipid synthesis intermediates, changes in sterol distribution, and lysosomal dysfunction.

13. 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

14. GARP is regulated by miRNAs and controls latent TGF-beta1 production by human regulatory T cells.

15. we investigated in detail miR-142-3 pregulation of GARP expression in regulatory CD25(+) CD4 T cells

16. 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.

17. 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

18. 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

19. the processing and expression of LRRC32

20. on chromosome 11q13.5 near the leucine-rich repeat containing 32 gene (LRRC32, also known as GARP) associated with asthma risk

Mouse (Murine) Leucine Rich Repeat Containing 32 (LRRC32) interaction partners

1. 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)

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.

3. GARP expression on MSCs contributed to their ability to inhibit T-cell responses in vitro.

4. 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.

5. 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.

6. GARP is a regulatory T cell specific cell surface molecule that mediates suppressive signals and induces Foxp3 expression