ライフサイエンスコーパス: collagen VII

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1 ysis bullosa caused by genetic deficiency of collagen VII.

2 trimerization of collagen VI, as well as in collagen VII.

3 5 and part of collagen IV, and disassembling collagen VII.

4 ment mediate antiparallel dimer formation of collagen VII.

5 each representing one antiparallel dimer of collagen VII.

6 velop in RDEB patients lacking expression of collagen VII altogether.

7 vitro at 2 wk of incubation for collagen IV, collagen VII, and laminin 5, and through 5 wk for epider

8 marked reductions in procollagens I and III, collagen VII, and the fibrillin-rich microfibrillar appa

9 Laminin-332 (formerly laminin-5) and collagen VII are basement membrane proteins expressed at

10 t showed negative staining for laminin 5 and collagen VII, but interrupted linear basal staining for

11 shown that it is required for the loading of collagen VII, but not collagen I, into COPII-coated tran

12 ss the role of the basement membrane protein collagen VII (COL7A1) in wound healing.

13 Cells devoid of collagen VII did not form tumors in mice, whereas those

14 rovided direct evidence for the existence of collagen VII dimers, but the dynamic process of dimer fo

15 Collagen VII expressed by intradermally injected mesench

16 py and immunohistochemistry for collagen IV, collagen VII, fibronectin, and laminin.

17 in mice, whereas those retaining a specific collagen VII fragment (the amino-terminal noncollagenous

18 tumor progression, which led us to subject a collagen VII hypomorphic mouse model of RDEB to chemical

19 on and therapeutic introduction of exogenous collagen VII in a preclinical model.

20 basement membrane, and diffuse staining for collagen VII in the superior stroma subjacent to the bas

21 To study the role of collagen VII in these cancers, we examined Ras-driven tu

22 tracellular cues, or whether laminin-332 and collagen VII interact together in this process remains u

23 sis in transformed cells lacking laminin-332/collagen VII interaction in a manner independent of cell

24 ion in our studies suggests that laminin-332/collagen VII interaction promotes epidermal carcinogenes

25 ed NC1 expression restored tumorigenicity to collagen VII-null epidermis in a non-cell-autonomous fas

26 n had significant effect on the abundance of collagen VII or its mRNA.

27 Expression of either collagen VII or the noncollagenous (NC1) fragment derive

28 at we define as an intermediate half-life of collagen VII, our study challenges the view of the derma

29 enic properties, but whether laminin-332 and collagen VII promote SCC tumors by providing adhesion or

30 Tumor-stroma interactions mediated by collagen VII thus promote neoplasia, and retention of NC

31 A similar in vivo stability of collagen VII was observed in the skin, tongue, and esoph

32 on of laminin, collagen IV, fibronectin, and collagen VII was performed.

33 t on the stromal surface in all samples, and collagen VII was present in four of five samples.

34 binding of all analyzed mutants to wild type collagen VII were different from those for binding betwe

35 Laminin, collagen IV, and collagen VII were usually either not present or were pre

36 C carcinogenesis/invasion through binding to collagen VII, which in turn, led to phosphoinositol-3-ki

37 with interrupted triple helices, as well as collagens VII, XIII, XXIII, and XXV, were found to conta

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