Leucine-Rich Repeats and Immunoglobulin-Like Domains 1 (Lrig1) ELISA试剂盒

Human Leucine-Rich Repeats and Immunoglobulin-Like Domains 1 (Lrig1) interaction partners

1. LRIG1 exerts important tumor-suppressive effects in EGFR-mutant NSCLC.

2. proposed LRIG1 protein interaction network

3. MiR-183 overexpression promoted radioresistance of glioblastoma via down-regulating LRIG1 and increasing the activity of EFGR/Akt.

4. LRIG1 is a negative regulator of RET2A and RET2B and is also downregulated in papillary and medullary thyroid carcinoma

5. LRIG1 expression in human GC tissues is inversely correlated with miR-20a and EGFR.

6. Role of LRIG1 in cancer [review]

7. LRIG1 expression may represent a barrier to EMT

8. LRIG1 role in the atrophic epidermis

9. Downregulation of LRIG1 expression in oral verrucous carcinoma tissue is reported.

10. LRIG1, as a negative mediated gene of tumor, can inhibit biological function of PAs via inhibiting PI3K/AKT and Ras/Raf/ERK pathways, and it might be a new target for gene therapy ofPituitary adenomas

11. LRIG1 and Fascin-1 were differently expressed in cancer and normal lung tissue in patients with NSCLC, which could be a biomarker for mediastinal lymph node metastasis in NSCLC patients.

12. Results suggest that the LRIG1could negatively control MRP-1 and the apoptosis to improve the sensitivity of VP16-related chemotherapy.

13. ERa-dependent expression of LRIG1 dampens ErbB3 signaling in luminal breast cancer cells, and by blocking ERa activity with fulvestrant, LRIG1 is decreased thus permitting ErbB3 accumulation, enhanced ErbB3 signaling to cell survival pathways

14. These findings demonstrate that LRIG1 is an independent prognostic factor in patients with non-small cell lung cancer

15. LRIG1 expression was associated with pathological type, differentiation status, and stage of Non-small Cell Lung Cancer. The result showed that LRIG1 was an independent prognostic factor for OS of NSCLC patients.

16. The inhibitory effects of LRIG1 are most likely mediated by suppression of the EGFR/PI3K/AKT pathway and epithelial-mesenchymal transition (EMT) process.

17. LRIG1 can enhance chemosensitivity in glioblastoma by inhibition of BCL-2 and MnSOD

18. Results showed that leucine-rich repeats and immunoglobulin-like domains can reverse multidrug resistance in glioblastoma, by negatively regulating epidermal growth factor receptor.

19. MiR-20a mediated temozolomide-resistance in glioblastoma cells through negatively regulating LRIG1 expression.

20. Based on these results, we concluded that the upregulation of LRIG1 expression inhibited the EGFR signaling pathway, activated the mitochondrial pathway of apoptosis and eventually increased the sensitivity of bladder cancer cells to CDDP.

Mouse (Murine) Leucine-Rich Repeats and Immunoglobulin-Like Domains 1 (Lrig1) interaction partners

1. Lrig1 marks gastric corpus epithelial progenitor cells capable of repopulating the damaged oxyntic mucosa by differentiating into normal gastric lineage cells in mouse stomach.

2. findings reveal a novel and essential role of Lrig1 in regulating morphogenic events that shape the hippocampal circuits and establish that the assembly of TrkB with Lrig1 represents a key mechanism for understanding how specific neuronal populations expand the repertoire of responses to BDNF during brain development

3. LRIG1 role in the atrophic epidermis

4. LRIG1+ cells were found to re-populate the neo-epidermis on day 14, suggesting an important homeostatic role of LRIG1 in skin

5. a subset of human duodenal tumors exhibited features of LRIG1(-/-) adenomas, including loss of LRIG1, gastric metaplasia (MUCIN5AC and MUCIN6), and increased amphiregulin and Egfr activity.

6. LRIG1 regulates the postnatal development of ICC-DMP and ICC-SMP from smooth muscle progenitors in mice.

7. Loss of one Apc allele in Lrig1(+) cells results in inducible stem cell-driven model that recapitulates features of familial adenomatous polyposis.

8. At later stages, Lrig1 expression is sustained in non-sensory tissues, whereas Lrig2 levels are enhanced in neurons and sensory epithelia.

9. LRIG1 orchestrates corneal-tissue transparency and cell fate during repair via STAT3.

10. A review summarizes the data that LRIG1 is a ERBB negative regulator and tumour suppressor.

11. LRIG1 Loss of heterozygosity (LOH) is frequent across cancers and its loss is an early event in the development of human squamous carcinomas.

12. The Lrig1, a negative-feedback regulator of the ErbB receptor family, is highly expressed by intestinal stem cells and controls the size of the intestinal stem-cell niche by regulating the amplitude of growth-factor signalling.

13. Study demonstrates that Lrig1 null mice develop duodenal adenomas, providing in vivo evidence that the ErbB negative regulator Lrig1 functions as a tumor suppressor.

14. Data show a dynamic expression pattern for diverse hair follicle (HF) stem cell markers Sox9 and Lrig1.

15. LIG-1 inversely correlated with proliferative ability of epidermal keratinocytes.

16. LRIG1-mediated receptor ubiquitination and degradation may contribute to the suppression of ErbB receptor function

17. Suppression of the negative regulator LRIG1 contributes to ErbB2 overexpression in breast cancer.

18. Our results suggest that Lrig1-positive cells constitute a previously unidentified reservoir of adult mouse interfollicular epidermal stem cells.