ライフサイエンスコーパス: keratin-1

1 ratins 6, 13, 14, and 19; and the absence of keratin 1.

2 n of the differentiation-associated proteins keratin 1/10, filaggrin, and loricrin by 80-95%.

3 plex virus thymidine kinase (HSV-TK) using a Keratin 1-15 (Krt1-15) promoter.

4 r subset involves the type II keratin chains keratin 1, 2e, 5, or 6 crosslinked to several protein pa

5 sion of several epithelial markers including keratins 1, 5, 10, and 14 while increasing expression of

6 y isolated infundibula were found to express keratins 1, 5, 6, 16, and 17, as determined by immunohis

7 amino acid substitution in the 1A domain of Keratin 1, a known target for human mutations that cause

8 We observed that keratin 1 and 10 end domains are likely to form a tetram

9 ssed markers of skin differentiation such as Keratin 1 and 10 instead of Keratin 12, a marker of corn

10 ith a significant decrease in deimination of keratin 1 and FLG, both important for epidermal differen

11 f HEKs and the Ca2+(o)-induced expression of keratin 1 and involucrin in HEKs.

12 attenuated the Ca2+(o)-induced expression of keratin 1 and involucrin in HEKs.

13 bition by epidermal growth factor suppresses keratin 1 and keratin 10 expression.

14 of human keratinocytes induces expression of keratin 1 and keratin 10 genes, early markers of termina

15 leading to the reduced tumorigenesis because keratin 1 and keratin 10, two keratins that indicate the

16 The pattern of expression of keratin 1 and keratin 5 indicated that epidermal differe

17 displaying reduced expression of Keratin 14, Keratin 1 and markers of proliferation.

18 Stratified cultures which made mouse keratin 1 and profilaggrin through passage 10 were induc

19 um with 0.15 mM calcium; expression of mouse keratin 1 and profilaggrin was lost by passage 15.

20 smoglein 1 (Dsg1), desmocollin 1 (Dsc1), and keratins 1 and 10 (K1/K10), in a dose-dependent manner i

21 SdrF bound human keratins 1 and 10 and adhered to keratinocytes and epith

22 ed expression of the differentiation markers keratins 1 and 10 induced by high calcium in the medium.

23 the A-FOS virus reversed the suppression of keratins 1 and 10 transcripts and protein, which is char

24 differentiation markers (e.g., profilaggrin, keratins 1 and 10) as well as certain pro-apoptotic gene

25 ns of the head and tail domains of epidermal keratins 1 and 10, based on all-atom 3D simulations of k

26 re altered in human skin diseases, including keratins 1 and 10, filaggrin, and loricrin.

27 ral markers of KC differentiation, including keratins 1 and 10.

28 o epidermal-like structures, which expressed keratins 1 and 6, filaggrin, loricrin and involucrin.

29 stimulating an early differentiation marker (keratin 1) and suppressing later markers (profilaggrin,

30 ifferentiation (such as desmoglein-1 [Dsg1], keratin-1, and loricrin) and abrogated MAL/SRF signaling

31 affecting the tail domains of keratin-10 or keratin-1, and Suzuki et al. expand the mutation spectru

32 one allele of the same lysine residue of the keratin 1 chain.

33 f the early (spinous) differentiation marker keratin 1 decreased in response to 1, 25(OH)2D3 over 12-

34 nondividing differentiated cells expressing keratin 1 did.

35 to the decreased expression of filaggrin and keratin 1 expression in adjacent NHKs.

36 Keratin 1 expression is reduced throughout days 19-28.

37 a more differentiated appearance as well as keratin 1 expression.

38 iation of primary keratinocytes, we measured keratin-1 expression and transglutaminase activity, mark

39 roM 8-Cl-adenosine for 24 h had no effect on keratin-1 expression or transglutaminase activity.

40 mutation in the exon 6 splice donor site of keratin 1 (G4134A) that segregates with a palmoplantar k

41 lizing a targeting vector based on the human keratin 1 gene (HK1.p53m).

42 t ras under the control of the keratin 10 or keratin 1 gene promoters, the formation of these lesions

43 Direct sequencing of the keratin 1 gene revealed a frameshift mutation in exon 9

44 kers to predict or diagnose graft rejection (Keratin 1 granzyme B, IL1beta).

45 ulated two early markers of differentiation, keratin 1 (K1) and keratin 10 (K10) but had a minimal ef

46 nt aggregates in these areas are composed of keratin 1 (K1) and keratin 10 (K10), and several K1 and

47 tissues have significantly higher levels of keratin 1 (K1) compared to normal breast tissues.

48 ent frameshift mutations in the V2 domain of keratin 1 (K1)).

49 expressing the early differentiation marker keratin 1 (K1).

50 Keratins 1 (K1) and 10 (K10) are the primary keratins ex

51 albumin (K212, K414, K199, and K351), human keratin 1 (K211 and K355), human keratin 10 (K163), bovi

52 olved in early KC differentiation, including keratin 1, keratin 10, and DSC-1, is reversed by p63 blo

53 of epidermal differentiation markers such as keratin 1, keratin 10, and loricrin, with or without the

54 rrant expression of differentiation markers, keratin 1, keratin 6, loricrin, and filaggrin in ML.myc2

55 esidues, which would spatially constrain the keratin 1/keratin 10 end domains to allow filament compa

56 ned the crystal structure of wild-type human keratin-1/keratin-10 helix 1B heterotetramer at 3.0 angs

57 n two early epidermal differentiation genes, Keratin 1 (KRT1) and ZNF750, facilitating R-loop removal

58 We identified a causal de novo mutation in keratin 1 (KRT1).

59 markers assayed by immunoblotting, including keratin 1, loricrin, filaggrin, involucrin, TGK, and SPR

60 for keratin 14 expression, and negative for keratin 1, loricrin, vimentin, and CD31.

61 and p27), a marker of early differentiation (keratin 1), mediators of apoptosis (caspases 3 and 8), a

62 nital ichthyosiform erythroderma also due to keratin 1 mutations, which show widespread and severe ep

63 sis, frequently associated with mutations in keratin 1 or 10 that result in disruption of the keratin

64 r epidermis of transgenic mice using a human keratin 1 promoter construct (HK1).

65 enic mouse model (HK1.bcl-2) using the human keratin 1 promoter to target the expression of a human b

66 howing that a polyarginine frameshift in the keratin-1 tail can also cause this disorder.

67 er keratin 14 and the differentiation marker keratin 1 was evident in Aurora-A(-/-) epidermis, there