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GLG1 encodes a transcription factor involved in the induction of genes regulated by oxygen, which is induced as oxygen levels fall. 再加上，我们可以发GLG1 抗体 (99) 和 GLG1 试剂盒 (3)和数多这个蛋白质的别的产品。
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Study identifies NRP2 (显示 NRP2 蛋白) and ESL-1 as targets for polysialylation in murine microglia and human THP-1 macrophages and reveals a striking convergence in the regulation of the two polysialylated acceptors in the course of inflammatory activation. A pool of polysialylated NRP2 (显示 NRP2 蛋白) and ESL-1 is assembled after injury or in culture and its shedding is an early response to lipopolysaccharide-induced activation of microglia.
A cell-intrinsic mechanism whereby haematopoietic cells limit proliferation within the bone marrow is repressed by E-selectin ligand 1 (ESL-1).
Data indicate that only the combined deficiency in PSGL-1 (显示 SELPLG 蛋白) and ESL-1 completely abrogated leukocyte recruitment.
Heterozygous deficiency of ESL-1 is associated with features of increased atherosclerotic plaque stability while complete deficiency of ESL-1 leads to embryonic lethality.
striking differences between the requirement of FucT-VII (显示 FUT7 蛋白) and C2GlcNAcT-I for Ligands for E-selectin (显示 SELE 蛋白) and P-selectin (显示 SELP 蛋白) expression in CD4 (显示 CD4 蛋白)+ T cells.
Data revealed interaction between Glg1 and Fgf18 (显示 FGF18 蛋白) both genetically and physically and reveals a novel regulatory mechanism for Fgf18 (显示 FGF18 蛋白) signaling involving Glg1 and Dlk (显示 DAPK3 蛋白).
E-selectin ligand-1 (ESL-1), P-selectin glycoprotein ligand-1 (PSGL-1 (显示 SELPLG 蛋白)), and CD44 (显示 CD44 蛋白) encompassed all endothelial-selectin ligand activity on neutrophils by using gene- and RNA-targeted loss of function.
Study identifies NRP2 (显示 NELL2 蛋白) and ESL-1 as targets for polysialylation in murine microglia and human THP-1 macrophages and reveals a striking convergence in the regulation of the two polysialylated acceptors in the course of inflammatory activation. A pool of polysialylated NRP2 (显示 NELL2 蛋白) and ESL-1 is assembled after injury or in culture and its shedding is an early response to lipopolysaccharide-induced activation of microglia.
Our results highlight the fact that interaction between APN (显示 ANPEP 蛋白) and ESL-1 could provide a fundamental mechanism underlying the anti-atherogenic properties of APN (显示 ANPEP 蛋白).
circulating prostate cancer cells' rolling capacity contributes to metastasis, and that is in part controlled by ESL-1.
Studies indicate that PSGL-1 (显示 SELPLG 蛋白), CD44 (显示 CD44 蛋白), and ESL-1 on mature leukocytes are physiologic glycoprotein ligands for endothelial P-selectin (显示 SELP 蛋白) and E-selectin (显示 SELE 蛋白).
expression of Cfr in the Golgi apparatus and on the plasma membrane is finely tuned through two distinct mechanisms for exhibiting different functions.
C2GnT1 (显示 GCNT1 蛋白) gene expression and the resulting C2-O-sLe(X) carbohydrates produced mediate the adhesive and invasive behaviors of human carcinomas which may influence their metastatic potential.
a novel variant of the GLG1 gene product called GLG2 is reported; genetic analysis suggests GLG1 & GLG2 are the products of a single gene, the mRNA of which can be processed by alternative splicing to generate different transcripts encoding GLG1 or GLG2
under hypoxia, ESL-1 is shed from activated hepatic stellate cells
a Golgi resident sialoglycoprotein that binds basic fibroblast growth factor
Golgi apparatus protein 1
, Golgi membrane sialoglycoprotein MG160
, golgi apparatus protein 1
, golgi glycoprotein 1
, golgi apparatus protein 1-like
, E-selectin ligand 1
, golgi sialoglycoprotein MG-160
, selectin, endothelial cell, ligand
, cysteine-rich fibroblast growth factor receptor
, Golgi sialoglycoprotein MG-160
, Latent TGF-beta complexed protein 1
, latent TGF-beta complexed protein (LTCP)