Gene name: integrin, beta 1 (fibronectin receptor, beta polypeptide, antigen CD29 includes MDF2, MSK12)
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PMID |
Sentence |
1 |
7608569
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The alpha 4 beta 1-integrin (CD49d, CD29) constitutively expressed on leukocytes regulates cell migration to inflammatory sites, cell activation, and development through its interactions with two alternate ligands, vascular cell adhesion molecule-1 (VCAM-1; CD106) expressed on cytokine-activated endothelium, dendritic and stromal cells, and the extracellular matrix protein fibronectin.
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2 |
7608569
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Another alpha 4-integrin receptor, alpha 4 beta 7, expressed on leukocytes also binds VCAM-1 and fibronectin (FN), and controls homing to mucosal tissues through its interactions with mucosal vascular addressin MAdCAM-1.
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3 |
7684344
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Aberrant distribution of CD4 and CD8 lymphocyte subsets in recent-onset IDDM patients.
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4 |
7684344
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The monoclonal antibodies 2H4 and 4B4 are specifically directed against CD45RA and CD29 antigens, respectively, which are expressed on both CD4+ and CD8+ lymphocytes.
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5 |
7684344
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CD45RA and CD29 are expressed on distinct subsets of CD4+ T-cells, whereas in both healthy subjects and IDDM patients, 2H4 and 4B4 labeling does not always differentiate two distinct CD8+ populations.
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6 |
7684344
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Before cyclosporin treatment, recent-onset IDDM patients had a significantly lower proportion of CD4+CD29+ cells than the healthy control subjects (42 +/- 11 vs. 52 +/- 9%, P < 0.004).
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7 |
7684344
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This imbalance corresponded to a significant increase in the CD4+ CD45RA+/CD4+ CD29+ ratio in the IDDM patients (1.37 +/- 0.93 vs. 0.78 +/- 0.36, P < 0.014).
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8 |
7684344
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The mean density of the CD45RA antigen (but not that of CD29) on both CD4+ and CD8+ cells was significantly higher in the IDDM patients before treatment than in the healthy control subjects.
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9 |
7684344
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Cyclosporin use was associated with a significant decrease in CD45RA antigen density on both CD4+ and CD8+ T-cells.
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10 |
7684344
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Aberrant distribution of CD4 and CD8 lymphocyte subsets in recent-onset IDDM patients.
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11 |
7684344
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The monoclonal antibodies 2H4 and 4B4 are specifically directed against CD45RA and CD29 antigens, respectively, which are expressed on both CD4+ and CD8+ lymphocytes.
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12 |
7684344
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CD45RA and CD29 are expressed on distinct subsets of CD4+ T-cells, whereas in both healthy subjects and IDDM patients, 2H4 and 4B4 labeling does not always differentiate two distinct CD8+ populations.
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13 |
7684344
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Before cyclosporin treatment, recent-onset IDDM patients had a significantly lower proportion of CD4+CD29+ cells than the healthy control subjects (42 +/- 11 vs. 52 +/- 9%, P < 0.004).
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14 |
7684344
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This imbalance corresponded to a significant increase in the CD4+ CD45RA+/CD4+ CD29+ ratio in the IDDM patients (1.37 +/- 0.93 vs. 0.78 +/- 0.36, P < 0.014).
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15 |
7684344
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The mean density of the CD45RA antigen (but not that of CD29) on both CD4+ and CD8+ cells was significantly higher in the IDDM patients before treatment than in the healthy control subjects.
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16 |
7684344
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Cyclosporin use was associated with a significant decrease in CD45RA antigen density on both CD4+ and CD8+ T-cells.
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17 |
9686681
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Furthermore, insulin stimulation led to downregulation of the levels of the alpha5- and beta1-integrin subunits in normal human fibroblasts but not in the patient's cells that lacked insulin receptors.
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18 |
10206487
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The role of CD8+ cells, cell degeneration, and Fas ligand in insulitis after intraperitoneal transfer of NOD splenocytes.
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19 |
10206487
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Cells expressing CD4, CD8, CD18, CD49d/CD29, CD44, CD54, CD80, CD86, CD106, CD11b/CD18 or DNA breaks were stained in the pancreases of female or male scid/ scid mice after adoptive transfer of lymphocytes from older than 12-week female nonobese diabetic (NOD) or Balb/c mice.
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20 |
10206487
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After intraperitoneal adoptive transfer of NOD splenocytes to female severe combined immunodeficiency (scid)/scid mice, in situ end labeling (ISEL)+ as well as CD80+ and CD86+ cell infiltrates appeared first in the blood vessel walls and pancreatic interstitial tissue at 2-3 weeks after transfer.
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21 |
10206487
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CD4+, CD8+, CD18+, CD44+, CD54+, and CD106+ cells then encircled and invaded some islets of the scid/scid mice 2 to 7 weeks after transfer.
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22 |
10206487
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Fas ligand was not present in Western blotting.
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23 |
10206487
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It is proposed that apoptosis commonly occurs in islet-infiltrating lymphocytes and that in the scid/scid adoptive-transfer model, the first islet-infiltrating cells are destroyed by programmed cell death independent of Fas ligand.
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24 |
11438667
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Smad proteins and hepatocyte growth factor control parallel regulatory pathways that converge on beta1-integrin to promote normal liver development.
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25 |
11438667
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Mice lacking one copy each of Smad2 and Smad3 suffered midgestation lethality due to liver hypoplasia and anemia, suggesting essential dosage requirements of TGF-beta signal components.
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26 |
11438667
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These pathways merge at the beta1-integrin, the level of which was increased by HGF in the cultured mutant livers.
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27 |
11438667
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HGF treatment reversed the defects in cell proliferation and hepatic architecture in the Smad2(+/-); Smad3(+/-) livers.
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28 |
11438667
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Smad proteins and hepatocyte growth factor control parallel regulatory pathways that converge on beta1-integrin to promote normal liver development.
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29 |
11438667
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Mice lacking one copy each of Smad2 and Smad3 suffered midgestation lethality due to liver hypoplasia and anemia, suggesting essential dosage requirements of TGF-beta signal components.
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30 |
11438667
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These pathways merge at the beta1-integrin, the level of which was increased by HGF in the cultured mutant livers.
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31 |
11438667
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HGF treatment reversed the defects in cell proliferation and hepatic architecture in the Smad2(+/-); Smad3(+/-) livers.
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32 |
15277376
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Increased serum levels of MRP-8/14 in type 1 diabetes induce an increased expression of CD11b and an enhanced adhesion of circulating monocytes to fibronectin.
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33 |
15277376
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Monocytes of type 1 diabetic patients displayed an increased adhesion to fibronectin in comparison with type 2 patients and healthy control subjects but had a normal expression of the FN binding integrins CD29, CD49a, CD49d, and CD49e (although CD11b and CD18 expression was increased).
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34 |
15277376
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MRP-8/14, which was increased in the sera of type 1 diabetic patients, induced healthy donor monocytes to adhere to FN and upregulate CD11b expression in a dosage-dependent manner.
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35 |
15358643
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In the placebo group, an increase in the number of subsets with the activated phenotype in both the CD4(CD29+) and the CD8 (CD11a+) compartments was noted during the course of the study.
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36 |
15358643
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However, in the placebo group the proportions of activated CD4 and CD8 cells increased over time.
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37 |
17460896
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The epithelial cells expressed PDX-1, PCNA, CK-7, CK-19, Nestin, Glut2, and Vimentin, but Insulin was undetected.
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38 |
17460896
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The cells expressed CD29, CD44, and CD166, but did not express CD11a, CD14, CD34, CD45, CD90, CD105, and CD117.
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39 |
18461147
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We show that BRCA1 mutant cancer cell lines contained a subpopulation of CD24+CD29+ or CD24+CD49f+ cells that exhibited increased proliferation and colony forming ability in vitro, and enhanced tumor-forming ability in vivo.
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40 |
18461147
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The purified CD24+CD29+ cells could differentiate and reconstitute the heterogeneity found in parental cells when plated as a monolayer.
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41 |
18461147
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Furthermore, CD24+CD29+ cells could form tubular structures reminiscent of the mammary ductal tree when grown in three-dimensional cultures, implying that these cancer cells maintain some of the characteristics of the normal stem cells.
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42 |
18461147
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We show that BRCA1 mutant cancer cell lines contained a subpopulation of CD24+CD29+ or CD24+CD49f+ cells that exhibited increased proliferation and colony forming ability in vitro, and enhanced tumor-forming ability in vivo.
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43 |
18461147
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The purified CD24+CD29+ cells could differentiate and reconstitute the heterogeneity found in parental cells when plated as a monolayer.
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44 |
18461147
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Furthermore, CD24+CD29+ cells could form tubular structures reminiscent of the mammary ductal tree when grown in three-dimensional cultures, implying that these cancer cells maintain some of the characteristics of the normal stem cells.
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45 |
18461147
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We show that BRCA1 mutant cancer cell lines contained a subpopulation of CD24+CD29+ or CD24+CD49f+ cells that exhibited increased proliferation and colony forming ability in vitro, and enhanced tumor-forming ability in vivo.
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46 |
18461147
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The purified CD24+CD29+ cells could differentiate and reconstitute the heterogeneity found in parental cells when plated as a monolayer.
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47 |
18461147
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Furthermore, CD24+CD29+ cells could form tubular structures reminiscent of the mammary ductal tree when grown in three-dimensional cultures, implying that these cancer cells maintain some of the characteristics of the normal stem cells.
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48 |
18566344
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Neurotrophin p75 receptor (p75NTR) promotes endothelial cell apoptosis and inhibits angiogenesis: implications for diabetes-induced impaired neovascularization in ischemic limb muscles.
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49 |
18566344
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The p75 receptor of neurotrophins (p75(NTR)), which is scarcely present in healthy endothelial cells (ECs), becomes strongly expressed by capillary ECs after induction of peripheral ischemia in type-1 diabetic mice.
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50 |
18566344
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Here, we show that gene transfer-induced p75(NTR) expression impairs the survival, proliferation, migration, and adhesion capacities of cultured ECs and endothelial progenitor cells (EPCs) and inhibits angiogenesis in vitro.
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51 |
18566344
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Moreover, intramuscular p75(NTR) gene delivery impairs neovascularization and blood flow recovery in a mouse model of limb ischemia.
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52 |
18566344
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In fact, p75(NTR) depresses the VEGF-A/Akt/eNOS/NO pathway and additionally reduces the mRNA levels of ITGB1 [beta (1) integrin], BIRC5 (survivin), PTTG1 (securin) and VEZF1.
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53 |
18566344
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Diabetic mice, which typically show impaired postischemic muscular neovascularization and blood perfusion recovery, have these defects corrected by intramuscular gene transfer of a dominant negative mutant form of p75(NTR).
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54 |
18566344
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Collectively, our data newly demonstrate the antiangiogenic action of p75(NTR) and open new avenues for the therapeutic use of p75(NTR) inhibition to combat diabetes-induced microvascular liabilities.
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55 |
19544426
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Subsequent single-cell cloning resulted in a homogeneous cell population with a CD29(+)CD44(+)Sca-1(+) surface antigen expression profile.
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56 |
19544426
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Our stage-specific approach successfully differentiated mesodermic mE-ASCs into definitive endoderm (cells expressing Sox17, Foxa2, GATA-4, and cytokeratin [CK]-19), then into pancreatic endoderm (cells expressing pancreatic and duodenal homeobox [PDX]-1, Ngn3, NeuroD, Pax4, and glucose transporter 2), and finally into cells expressing pancreatic hormones (insulin, glucagon, somatostatin).
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57 |
20158462
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After long term cryo-preservation hTGSCs expressed surface antigens CD29, CD73, CD90, CD105, and CD166, but not CD34, CD45 or CD133, which was typical for non-frozen hTGSCs.
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58 |
21099303
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Human umbilical cord matrix stem cells (hUCMSCs) were found to express CD29, CD44, CD73, CD90, CD105, smooth muscle actin, nestin, vimentin, proliferation marker Ki67 and embryonic markers Oct4, SSEA4.
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59 |
21099303
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These were found to be negative for CD33, CD34, CD45 and HLA DR.
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60 |
21099303
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Real time qPCR analysis of newly generated islets further demonstrated abundance of Pdx-1, Ngn3, insulin, glucagon and somatostatin transcripts.
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61 |
21099310
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In these clusters the expression of insulin, glucagon, and somatostatin genes is induced.
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62 |
21099310
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Human IPC lack expression of Von Willebrand Factor, CD31, CD34, CD45, and CK19 and CA19.9, demonstrating that hIPC are neither of hematopoietic, endothelial, nor of ductal origin.
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63 |
21099310
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The mesenchymal stem cells (MSC) markers CD105, CD90, CD73, CD44, CD29, and CD13 are expressed, as well as nestin and vimentin.
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64 |
21099310
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Also hIPC express the pericyte markers CD146, NG2, αSMA and PDGF-Rβ.
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65 |
21099310
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Immunoflowcytometry revealed that human islets contain 2.0 ± 0.8% of CD105/CD90 double-positive cells.
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