Publication for COL1A1 and COL11A1
| Species | Symbol | Function* | Entrez Gene ID* | Other ID | Gene coexpression |
CoexViewer |
|---|---|---|---|---|---|---|
| hsa | COL1A1 | collagen type I alpha 1 chain | 1277 | [link] | ||
| hsa | COL11A1 | collagen type XI alpha 1 chain | 1301 |
| Pubmed ID | Priority | Text |
|---|---|---|
| 31598423 | 1.00 | COL1A1, COL10A1 and COL11A1 were notably overexpressed in ESCC compared to normal tissues. |
| 0.96 | COL1A1, COL10A1 and COL11A1 were particularly up-regulated in ESCC tissues compared to normal controls, while COL4A4, COL6A5 and COL14A1 were notably down-regulated. | |
| 0.96 | COL1A1, COL10A1 and COL11A1 was particularly higher, and that of COL4A4, COL6A5 and COL14A1 was especially lower in tumor tissues, indicating their possible roles as diagnostic markers for ESCC. | |
| 0.94 | COL1A1, COL11A1, COL6A6 and COL19A1, were co-expressed with NETO1, NEUROD2 and NRG3, which are the genes involved in neural functions. | |
| 0.92 | COL1A1, COL10A1 and COL11A1 in TCGA and GEO. (J-O) Boxplots of three representative down-regulated genes, COL4A4, COL6A5 and COL14A1 in TCGA and GEO. | |
| 0.65 | COL1A1, COL10A1 and COL11A1 were notably overexpressed in ESCC compared to normal tissues. | |
| 0.64 | COL1A1, COL10A1 and COL11A1 ranked in the top five among the up-regulated DEGs in both datasets (Figs. 1D-1I), further presented by boxplots. | |
| 30723390 | 0.97 | COL11A1, THBS2, COL8A1, COL1A1, BGN, MMP2, PXDN, THY1, and TGFB1I1 was identified. |
| 0.97 | COL1A1, (e) COL1A2, (f) COL11A1, (g) MMP2, (h) PXDN, and (i) THY1. | |
| 0.97 | COL11A1, THBS2, COL8A1, COL1A1, BGN, MMP2, PXDN, THY1, and TGFB1I1. | |
| 0.93 | COL1A1, COL1A2, COL11A1, MMP2, PXDN, BGN, COL5A1, COL8A1, and TGFB1I1 indicated poor prognosis of the patients(P < 0.05). | |
| 0.93 | COL1A1, COL1A2, COL11A1, MMP2, PXDN, and THY1 was related to the poor prognosis of the disease. | |
| 0.93 | COL1A1, COL1A2, COL11A1, MMP2, PXDN, BGN, COL5A1, COL8A1 associated with the tumor stage as well as tumor patients' prognosis. | |
| 0.70 | COL1A1, COL1A2, COL11A1, MMP2, PXDN, BGN, and THY1(Fig. 5). | |
| 30948703 | 0.97 | COL1A1, COL3A1, COL1A2, COL5A2, FN1, THBS1, COL5A1, SPARC, COL18A1, and COL11A1) were identified via PPI network analysis. |
| 0.96 | COL1A1, COL1A2, COL5A2, COL11A1, COL18A1, FN1, and SPARC - were related to the OS of GC patients. | |
| 0.93 | COL1A1, COL3A1, COL1A2, COL5A2, FN1, THBS1, COL5A1, SPARC, COL18A1, and COL11A1. | |
| 0.89 | COL1A1, COL5A1, and COL11A1, was upregulated in renal cell carcinoma compared with levels in controls. | |
| 0.88 | COL1A1, COL1A2, COL5A2, COL11A1, COL18A1, FN1, and SPARC was associated with poor OS of GC patients. | |
| 0.64 | COL1A1, COL3A1, COL1A2, COL5A2, FN1, THBS1, COL5A1, SPARC, COL18A1, and COL11A1. | |
| 27356888 | 0.97 | COL1A1 and COL11A1 were included (Fig. 2A). |
| 0.94 | COL1A1 and COL11A1 may be important gene signatures contributing to OA development via involvement in ECM-receptor interactions and focal adhesion. | |
| 0.91 | collagen type I alpha 1 (COL1A1), COL1A2, COL3A1, COL4A2, integrin alpha 1, COL4A1, biglycan and COL11A1. | |
| 0.90 | COL1A1 and COL11A1, were predominantly enriched in the ECM-receptor interaction and focal adhesion pathways. | |
| 0.57 | COL1A1 and COL11A1 may be important gene signatures in OA development via involvement in the pathways of ECM-receptor interactions and focal adhesions. | |
| 25860484 | 0.97 | COL1A1, COL1A2, COL5A2, COL11A1, and SPP1) were most significantly altered and were all involved in the ECM-receptor interaction and focal adhesion pathway (Table 2). |
| 0.96 | COL1A1, COL1A2, COL5A2, and COL11A1 belong to the collagen protein family, essential structural components of ECM. | |
| 0.93 | COL1A1, COL1A2, COL5A2, COL11A1, DSG3, ACHE, SERPINE1, SERPINB2, CXCL5, MMP1, PLAU, SPP1, GJB2, CLDN2, CDKN2A, CENPF, MAD2L1, and NCAM1), most of which (17 out of 18) were up-regulated in gastric cancer tissues (Fig 4). | |
| 0.90 | COL1A1, COL1A2, COL5A2, COL11A1, and SPP1) co-regulated by both TFs and miRNAs participated in ECM-receptor interaction and focal adhesion pathways. | |
| 30237810 | 0.97 | COL1A1, COL5A1, COL5A2, COL10A1 and COL11A1, were also responsible for encoding collagens, which are the most abundant proteins in the ECM. |
| 0.97 | COL1A1, COL5A1, COL5A2, COL10A1 and COL11A1. | |
| 0.57 | COL1A1, COL5A1, COL5A2, and COL11A1), integrin (ITGA6), tenascin (TNXB) and fibronectin (FN1). | |
| 19388929 | 0.97 | COL11A1, COL1A1, CD44, SELE, LAMA3 and ITGA9 were significantly downregulated by PT-100 in cocultured osteoclasts. |
| 0.95 | COL11A1, COL1A1, COLA4A2), laminins (LAMA3, LAMB1) and other adhesion molecules including E-selectin (SELE), CD44 and ITGA9. | |
| 27843486 | 0.97 | COL1A1, COL5A1, and COL10A1, and 8 genes with degree of node 3 are FBN1, LUM, LRRC15, COL11A1, THBS2, SPARC, COL1A2, and FAP, respectively. |
| 0.93 | COL1A1, COL5A1, and COL11A1. | |
| 28586059 | 0.96 | COL1A1, COL11A1 and COL5A2) and neuroactive ligand-receptor interaction (dM3; P=9.49x10-4; Table IVB). |
| 0.94 | COL1A1, COL1A2, COL3A1, COL5A2, COL6A1, COL6A2, COL6A3, COL11A1, COL12A1 and ITGA4 may interact with each other. | |
| 0.88 | COL1A1, COL11A1 and COL5A2), G-protein coupled receptor protein signaling pathway (dM3; P=7.27x10-4) and wound healing (dM4; P=1.56 x10-4; Table IVA). | |
| 22208948 | 0.96 | COL11A1, THBS2, COL5A2, COL5A1, VCAN, COL1A1, COL3A1, FN1,SULF1, FBN1, ASPN, SPARC, CTSK, MMP2, BGN, LUM, LOXL2, COL6A3, TIMP3, CDH11, SERPINF1, EDNRA, ACTA2, PDGFRB, SNAI2, LGALS1, GLT8D2, NID2, PRRX1) belong to the set of 64 genes in Table 1 (P = 10-27), as well as VIM (vimentin). |
| 28856171 | 0.96 | COL1A1, COL2A1, COL11A1, COL11A2, COL12A1, COL14A1) did not have a significant independent association with tendon injury, even though they have been linked to other musculoskeletal injuries (eg, COL1A1 Sp1 with ACL tears, shoulder dislocations, osteogenesis imperfecta, and lumbar disc disease; COL2A1 with spondyloepiphyseal dysplasia). |
| 28881680 | 0.96 | COL11A1 and COL1A1 belong to fibrillar collagen. |
| 28331057 | 0.95 | Col11a1 and Col8a2, while Col1a1 transcript was ranked 7th (Fig. 1B). |
| 0.93 | COL11A1 and COL1A1 levels were significantly increased by TGFbeta2 treatment (Fig. 5B). | |
| 0.90 | COL11A1 appeared to have very little colocalization with COL1A1. | |
| 0.84 | COL11A1 and COL1A1 in the fibrotic phase of conjunctival wound healing | |
| 0.83 | COL1A1 and low COL8A1/high COL1A1 co-immunolabellings, respectively; inset (ii) left, second image, shows a magnified image of the boxed area co-immunolabelled for COL8A1 and COL11A1; inset (ii) right, second image, shows a magnified image of the boxed area co-immunolabelled for COL11A1 and COL1A1; inset (ii), fourth image, shows a magnified overlay image of the boxed area co-immunolabelled for all three collagens. | |
| 0.77 | COL11A1 and COL1A1 in human fibroblasts treated as indicated for 72 h. Three independent sets of experiments are shown. | |
| 0.71 | COL11A1 (green) and COL1A1 (magenta). | |
| 30542454 | 0.95 | COL1A1, COL1A2, CTSK, ITGB4, TIMP1, ITGA11, COL11A1, MYBL2, KPNA2, AURKA, TPX2 and CDC20. |
| 0.94 | COL1A1, (D) CDC20, (E) MYBL2, (F) POSTN, (G) COL11A1, (H) TPX2, (I) COL3A1, (J) TIMP1, (K) DNALI1, (L) DNAH6, (M) CTSK, (N) DYNC2H1, (O) DNAH12 and (P) WDR78, on the survival of lung cancer patients. | |
| 0.91 | COL1A1, COL1A2, CTSK, ITGB4, TIMP1, ITGA11, COL11A1, MYBL2, KPNA2, AURKA, TPX2 and CDC20) were identified as hub genes in smoking-associated lung cancer. | |
| 0.63 | COL1A1, COL1A2, cathepsin K (CTSK), integrin subunit beta 4 (ITGB4), tissue inhibitor of metalloproteinases 1 (TIMP1), ITGA11, COL11A1, MYB proto-oncogene like 2 (MYBL2), karyopherin subunit alpha 2 (KPNA2), aurora kinase A (AURKA), TPX2, microtubule nucleation factor (TPX2) and cell division cycle 20 (CDC20) were identified as key upregulated genes in smoking-associated lung cancer (Fig. 2A and B). | |
| 29196464 | 0.95 | COL11A1, COMP, VCAN, FN1, COL1A1 and CTSB have all been associated with cancer progression, poor prognosis and malignant cell invasion in ovarian and/or other cancers. |
| 29360819 | 0.94 | Col1a1 and Col11a1 in colon cancers and matched normal colon with quantification of the area (%) of the microarray core demonstrating positive staining (n=20 per analysis). |
| 30828485 | 0.94 | COL1A1, COL1A2, COL2A1, COL3A1, COL5A1, COL5A2, COL6A1, COL8A1, COL11A1, and COL24A1. |
| 26870242 | 0.93 | COL1A1, COL5A2, THBS2, COL11A1 and COL5A1) were involved in the ECM-receptor interaction pathway. |
| 0.78 | COL1A1, COL5A2, thrombospondin 2 (THBS2), COL11A1 and COL5A1] were predicted to participate in the pathway. | |
| 31427586 | 0.93 | COL1A1 variants (3/5), 100% for spondyloepiphyseal dysplasia congenita with a COL2A1 variant (1/1), 100% for Stickler syndrome with COL11A1, COL11A2 variants (2/3, 1/3), 33% for CHARGE syndrome with a CHD7 variant (1/3), 100% for Jervell and Lange-Nielsen syndrome with a KCNQ1 variant (1/1), 100% for auditory neuropathy with a OPA1 mutation (1/1), and 89% for Pendred syndrome with SLC26A4 variants (32/36). |
| 29601813 | 0.92 | COL1A1 expression was highest by ~2-3 orders of magnitude when compared to COL11A1 and by ~6 orders of magnitude when compared to COL3A1. |
| 0.85 | COL1A1, COL3A1, and COL11A1 were not affected by peptide motif, fiber stiffness, or loading. | |
| 19652764 | 0.92 | COL11A1, COL1A1, COL3A1, COL1A2, COL15A1). |
| 29358879 | 0.91 | COL11A1, BMP7, MMP12, LAMC2, COL27A1, ITGB4, PDGFRA, ADAMTS2, IBSP, COL10A1, COL7A1, MMP11, MFAP2, MMP1, and COL1A1. |
| 0.83 | COL11A1, BMP7, MMP12, LAMC2, COL27A1, ITGB4, PDGFRA, ADAMTS2, IBSP, COL10A1, COL7A1, MMP11, MFAP2, MMP1, and COL1A1. | |
| 30572540 | 0.91 | COL1A1, COL10A1, COL11A1, CCL20, and CXCL5, could be used not only for the differential diagnosis of PTC from normal samples, but also for the differential diagnosis of TCPTC from cPTC samples. |
| 23936839 | 0.90 | collagen type I, alpha 1 (COL1A1; 1.62-fold change), collagen type XI, alpha 1 (COL11A1; 1.82-fold change), and collagen type XIV, alpha 1 (COL14A1; 2.06-fold change), was upregulated by PC. |
| 20952505 | 0.89 | COL11A1, COL1A1, COL3A1, CALD1, and TNNC1). |
| 27626164 | 0.88 | COL1A1 and COL11A1 were also behaved up-regulation trend in cancer, except FLNC. |
| 0.55 | COL1A1 and COL11A1 in tumor tissues were obviously higher than non-tumor tissues (Figure S3B-S3D), which illustrates that tumor invasion and metastasis related pathways were up-regulated in tumor compared with non-tumor tissues, especially for FLNC.These results further demonstrated that the up-regulation of FLNC is a common phenomenon in HCC and FLNC might have the potential to be used as a biomarker for HCC diagnosis. | |
| 29844680 | 0.88 | COL11A1, COL4A1, COL5A2, COL5A1, COL1A1, COL1A2, COL5A3 and THBS2) and 46 edges with a score of 8.5 was detected by MCODE. |
| 22550553 | 0.87 | COL1A1, COL9A1, COL9A2, COL9A3, COL11A1, COL11A2), vitamin D receptor (VDR), matrix metalloproteinases (MMP2, MMP3, MMP9), interleukins (IL1, IL2, IL18R1, IL18RAP), cyclooxygenase-2 (COX2) and cartilage intermediate layer protein (CILP) have been reported with different pathologic changes of disc degeneration and clinical phenotypes. |
| 32058995 | 0.87 | COL1A1, COL11A1, COL4A6, and THBS2) are involved in both pathways. |
| 23372777 | 0.83 | COL1A1, COL1A2 and COL3A1, other collagens (COL4-6A2 and COL12A1), and ECM genes (BGN, VCAN, DCN, SPARC, SPON1 and THBS1) were up-regulated in PanIN-X lesions and PDACs; in PDACs, stromal involvement was characterised by an even higher diversity of collagens (COL10A1, COL11A1, COL14-16A1 and COL18A1 were additionally seen), and even higher expression than in PanIN-X lesions of the ECM genes mentioned above. |
| 23555081 | 0.77 | COL1A1; 1.66-fold change), and collagen type XI alpha-1 (COL11A1; 1.50-fold change), was upregulated by PC (Table 2). |
| 26351771 | 0.50 | collagen type I alpha 1 (COL1A1); COL5A1; COL11A1; COL14A1; COL16A1; contactin 1; connective tissue growth factor (CTGF); catenin, alpha 1; catenin Delta 2; integrin beta 2 (ITGB2); kallmann syndrome 1 sequence (KAL1); laminin alpha 3 (LAMA3); matrix metallopeptidase 2 (MMP2); MMP3; MMP7; MMP12; MMP13; selectin E; secreted protein acidic, cysteine-rich (SPARC); transforming growth factor, beta-induced; Thrombospondin 3 (THBS3); and Versican (VCAN). |
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