Disease relevance of Krt13

• In PDV, PDVCM1, PDVCM2, and PDVCV1 carcinomas the overall expression of K13 is higher than that of K8 [1].
• Beginning with very early papillomas (after 10 wk of promotion), expression of alpha6beta4 in suprabasal cells and small, focal staining for keratin 13 (K13) were seen in some tumors [2].
• The identical situation is encountered in DMBA TPA-induced moderately differentiating epidermal squamous cell carcinomas with compartmentalized K13 expression [3].
• DNAseI hypersensitivity in K13-expressing tissues was, however, independent of an active transcription of the gene in differentiating cells or transcriptional inertia in basal cells [3].
• As seen in SQUU-B cell line, SQUU-B of the cervical lymph node metastasis did not exhibit CK13, 14, or 16 [4].

High impact information on Krt13

• Constitutive NF-kappaB activation, normal Fas-induced apoptosis, and increased incidence of lymphoma in human herpes virus 8 K13 transgenic mice [5].
• In tumors, loss of TGF-beta is controlled at the posttranscriptional level and is associated with expression of keratin 13, a documented marker of malignant progression [6].
• When tumors first appeared at 8 weeks after promotion, high risk papillomas demonstrated basal and suprabasal alpha 6 beta 4 expression, loss of keratin 1, and aberrant expression of keratin 13 [7].
• By 33 weeks, alpha 6 beta 4 suprabasal expression continued to distinguish groups at higher risk for malignant conversion, but keratin 13 was expressed in all groups [7].
• The predominance of alpha 6 beta 4 in the proliferating cells during progression is associated with decreased expression of keratin 13 in carcinomas [8].

Chemical compound and disease context of Krt13

• A monoclonal IgG1 anti-idiotype, specific for the K13 polysaccharide combining site of a protective IgM idiotype, primed for protection against intraperitoneal infection with live E. coli K13 following K13 injections at four as well as 12 weeks of age, the K13 polysaccharide alone did not immunize and protect [9].

Biological context of Krt13

• To investigate whether the aberrantly expressed K13 gene falls into the category of those genes, reporter gene constructs of K13-RARE variants in which either the initial or the terminal thymidine of the second half-motif was replaced by adenine were transfected into epidermal cell lines [10].
• In an approach to unravel regulatory DNA sequence elements involved in the tissue-specific and aberrant K13 expression, the 5'-flanking region of the gene was analyzed with regard to potential methylation sites and DNase hypersensitive regions [3].
• These results suggest that the loss or down-regulation of CK13, 14, or 16 is related to the invasive and metastatic ability of cancer [4].
• The benign tumours that arose had several hallmarks of tumours at a high risk of malignant progression, including suprabasal cell proliferation and heterogeneous expression of keratin 13 [11].
• Our results suggest that K13 may provide a marker for malignant conversion in the mouse two-stage skin carcinogenesis model and may be especially suited for studies of gene expression regulation [12].

Anatomical context of Krt13

• In tumors induced by the cell lines upon injection in mice, K8 is found in the less differentiated regions as opposite to K13, restricted to the differentiating areas of the tumors [1].
• This indicates that the activation of one of the members of the ras gene family is not a general prerequisite for the aberrant expression of K13 in mouse epidermal keratinocytes [13].
• Reverse transcription-polymerase chain reaction was performed to detect expression of desmosome and hemidesmosome-associating adhesion molecules, keratin 13, and keratin14 [14].
• 211At was bound to polymer microspheres and its efficacy was compared with the beta-emitting 32P and 90Y colloids for the treatment of intraperitoneally growing K13 hybridoma tumors in mice [15].

Associations of Krt13 with chemical compounds

• As in cultured primary keratinocytes from normal internal stratified epithelia, the in vitro expression of K13 in transformed epidermal cell lines can be induced either by Ca2+ or by retinoic acid (RA) [10].
• Induction of differentiation may be mechanism of the response to RE-80 in vivo since carcinoma cells expressing K13 did not incorporate bromodeoxyuridine and were on a terminal pathway [16].
• K13 induction in vitro was correlated with response to retinoid in vivo [16].
• The results showed a significantly higher protective effect for the antibodies against the K1 and K13 antigens than for the antibodies against the O2 and O6 lipopolysaccharides [17].
• Such conjugations were performed using cyanogen bromide for the K1 antigen and bisdiazobenzidine for the K13 antigen [17].

Regulatory relationships of Krt13

• With that purpose, we analyzed the keratin profiles of 16 DMBA-induced hamster skin tumors using monospecific antibodies against K1 and K13 [18].

Other interactions of Krt13

• Restriction mapping and sequencing data indicate that they encode the mouse K15 and K13 [19].
• On the other hand, almost all SCCs showed suprabasal staining for alpha6beta4 and widespread cyclin D1 and K13 expression, whereas only about half showed positive focal staining for GGT activity [2].
• We have found that the promoter of the K13 gene contains a sequence element GGTTCA(N)5TGTTCT, in the following referred to as K13-RARE, that is highly related to the natural retinoic acid responsive element (RARE) of the retinoic acid receptor beta 2 gene [10].
• Low frequency of codon 61 Ha-ras mutations and lack of keratin 13 expression in 7,12-dimethylbenz[a]-anthracene-induced hamster skin tumors [18].
• These results strongly suggest that the sequence element around the demethylated M1 site is involved in a multi-level control mechanism mediating the selective expression of the K13 gene in internal squamous epithelia and in DMBA/TPA-induced epidermal tumors [3].

Analytical, diagnostic and therapeutic context of Krt13

• All cell lines exhibit a concentration optimum for the stimulatory agents; however, the degree of maximal K13 expression varies considerably among the individual cell lines and shows a striking correlation with the reported tumorigenicity of the lines after transplantation to animals [20].
• K13 and K1 expression in papillomas was studied using immunoblotting and immunostaining of consecutive sections, as previously described [21].
• Combined analysis of the grafts by western blotting of extracted keratins and immunofluorescence studies of frozen sections with a K13-monospecific antibody revealed K13 expression in all v-Ha-ras-induced papillomas and absence of this keratin in all control grafts [22].
• METHODS: Ultrastructures of GE1 cells were observed and immunohistochemistry was used to detect keratin 4, keratin 13, and desmoglein expression [14].
• Indirect immunofluorescence indicated induction of a differentiation-associated keratin of internal stratified epithelia, K13, and inhibition of the differentiation-associated epidermal keratin K1 [16].

References