Disease relevance of KRT17

• This mutation predicts the substitution of asparagine by aspartic acid in codon 109 (N109D) located in the second half of the keratin 17 1A domain, where similar mutation in keratin 5 is associated with the mild Weber-Cockayne form of epidermolysis bullosa simplex [1].
• Keratins (K16 and K17) as markers of keratinocyte hyperproliferation in psoriasis in vivo and in vitro [2].
• The results demonstrate that both K16 and K17 expression are features of acute irritant contact dermatitis reactions, but suggest that the factors which influence and control their expression differ [3].
• K17 and K5/6 were present in cysts and squamous metaplasia of goitres, and focally in papillary but only exceptionally in follicular carcinoma in areas of squamous differentiation and tumour cells in desmoplastic stroma [4].
• METHODS: Expression of CK5/6 or CK17 was analyzed by immunohistochemistry in 195 women with breast cancer [5].

Psychiatry related information on KRT17

• Baseline currents were similar for both sexes: 21.4 +/- 1.6 mA for pain threshold and 39.1 +/- 2.3 mA for pain tolerance [6].
• RESULTS: A total of 43.4, 39.1, and 17.5% of respondents without disabilities were active at a recommended level, insufficiently active, and inactive, respectively, taking into account nonoccupational physical activities [7].
• METHODS: Nine patients with PC (three each with frontotemporal dementia, corticobasal degeneration [CBD], and primary progressive aphasia [PPA]) and five healthy subjects underwent (1)H-CSI [8].
• Interestingly, the cortical response time of the medial hamstring and the medial quadriceps muscles in the isokinetic group slowed significantly, by 39.1 and 32.4 msec, respectively, after 6 weeks of training [9].
• The densities of Pick bodies (PB), Pick cells (PC), senile plaques (SP) and neurofibrillary tangles (NFT) in the frontal and temporal lobe were determined in ten patients diagnosed with Pick's disease (PD) [10].

High impact information on KRT17

• Patients were categorized according to the hematocrit on admission (5.0 to 24.0 percent, 24.1 to 27.0 percent, 27.1 to 30.0 percent, 30.1 to 33.0 percent, 33.1 to 36.0 percent, 36.1 to 39.0 percent, or 39.1 to 48.0 percent), and data were evaluated to determine whether there was an association between the use of transfusion and 30-day mortality [11].
• Keratin 16 and keratin 17 mutations cause pachyonychia congenita [12].
• Here, we show that a heterozygous missense mutation in the helix initiation motif of K17 (Asn92Asp) co-segregates with the disease in this kindred [12].
• PC2, the high-molecular weight constituent of the potent USA transcriptional coactivator fraction, was identified as a Mediator-like complex [13].
• Additionally, group C monoclonal antibody PC-2 was unique in that it showed partial reactivity against the clonable progenitor for the erythroid series (BFU-E) [14].

Chemical compound and disease context of KRT17

• However, there was no change in serum nitrogen oxide levels (42.1 +/- 24.5 vs. 39.1 +/- 16.6 micromol/liter, p = 0.61), nor was there an effect of L-arginine on flow-mediated dilation during hyperemia (3.8 +/- 3.0% vs. 4.9 +/- 4.8%, p = 0.53) compared with placebo [15].
• Among seven schizophrenic patients subject to water intoxication (six men and one woman, mean age 39.1 +/- 6.9 years), we measured serum sodium, plasma arginine vasopressin, and urine osmolality at 7 a.m. and 4 p.m. on eight consecutive Thursdays [16].
• To this end, MCF-7 cells as well as a series of breast carcinomas (n = 10; fresh frozen as well as formalin fixed and paraffin embedded) were stained using a panel of different antibodies directed against the Ki67-Ag (DAKO/PC, MIB-1, Ki-S5, and poly-Ki67) for a 3-parameter cytokeratin/Ki67-Ag/DNA FCM analysis [17].
• In singleton pregnancies the gestational length and birth weight of the newborn infants were greater in the steroid treatment group (N = 23, 39.1 +/- 0.3 weeks, 3,460 +/- 119 gm) than in the ritodrine group (N = 24, 37.7 +/- 0.4 weeks, 3,106 +/- 118 gm) [18].
• 14 full-term neonates with a mean birth weight of 3,240 g and a mean gestational age of 39.1 weeks were administered metoclopramide (MTC), a specific dopamine antagonist, in a dose of 0.1 mg/kg/day to treat delayed gastric emptying, regurgitation and abdominal distension [19].

Biological context of KRT17

• From these findings and from immunohistological observations, CK 17 synthesis seems to be a marker of basal cell differentiation in complex epithelia and therefore indicative of a certain type of epithelial "stem cells" [20].
• Because of its unusual expression pattern in normal and diseased states and because of the potential importance of CK 17 in tumor diagnosis, we have characterized the gene(s) and its cDNA-derived amino acid sequence [20].
• A cDNA clone encoding CK 17 was isolated from a HeLa cDNA library and used for the determination of the amino acid sequence, for studies of expression and for the screening of human genomic libraries [20].
• The 5 kbp CK 17 gene with 8 exons and 7 introns encodes a polypeptide of 432 amino acids with a calculated molecular weight of 48,000 [20].
• Only one of these loci contains the functional CK 17 gene which is located only approximately 5 kbp 5'-upstream of the CK 16 gene, whereas the other two contain unprocessed CK 17 pseudogenes [20].

Anatomical context of KRT17

• They further suggest that when present at sufficiently high intracellular levels, K16, along with K6 and K17, appear capable of inducing a reorganization of keratin filaments in the cytoplasm of skin epithelial cells [21].
• Among the members of the cytokeratin (CK) subfamily of intermediate filament (IF) proteins, CK 17 is remarkable as it is normally expressed in the basal cells of complex epithelia but not in stratified or simple epithelia [20].
• Immunoreactivity for CK5/14 and CK17 involved all layers of the epithelium [22].
• Keratin 17 (K17) is a differentiation-specific keratin expressed in the nail bed, hair follicle, sebaceous gland and other epidermal appendages [23].
• OBJECTIVE: To identify the HLA DR B1*04, *07-restricted T cell epitopes on Keratin 17 [24].

Associations of KRT17 with chemical compounds

• Multiple acetylated lysine residues have been identified in the N-terminal domain of H2B (K6, K11, K16, K17, K21, and K22), but little is known about how these modifications regulate transcription [25].
• The result that RA induced expression of keratins K6, K16, and K17, as commonly expressed in hyperproliferative epidermis, is consistent with the notion that retinoids increase epidermal cell proliferation in the basal and/or lower spinous layers [26].
• In summary, our results document that acute or chronic barrier disruption leads to expression of keratins K6, K16, and K17 and to a premature expression of involucrin [27].
• The average molecular areas at this inner surface are Spl = 68.5 A2/molecule for phospholipids and Sc= 39.1 A2/molecule for cholesterol [28].
• Labeling of metabolic pool with 14C-adenine revealed a mean decrease in the adenylate energy charge of 2.0 /+- 0.4% in 12 of 16 stored PC, with a lower ATP and higher hypoxanthine labeling in stored as compared to fresh platelets [29].

Other interactions of KRT17

• Biochemically, using 2-DE and immunoblotting, stratified epithelial keratins K5/K14 and large amounts of K17 were present in all cases [30].
• Long-range restriction mapping analysis of clone 211F11 and of two smaller YAC clones that were also isolated with KRT13-specific primers, suggests that KRT13, 14, 15, 16 and their linked type I genes KRT17 and 19, are contained in less than 150 kb of genomic DNA [31].
• The comedone wall showed a pattern of keratin expression similar to that of the upper follicle, except that there was, in addition, expression of keratins K6 and K16 suprabasally, and panepithelial expression of K17 in the comedone wall [32].
• The monophasic tumors showed limited positivity for complex epithelial keratins: K14 (28%) and K17 (10%) [33].
• It has been demonstrated that PC-2 is associated with germline mutations in the keratin 17 (K17) gene and in its expression partner keratin 6b [34].

Analytical, diagnostic and therapeutic context of KRT17

• Northern blot hybridization experiments showed a restricted pattern of CK 17 gene expression, supporting the notion that CK 17 synthesis is essentially regulated at the transcriptional level [20].
• Recently we demonstrated that the keratin 17 (K17) content exceeded the K16 content in most follicular tumors, in comparison with non-follicular epithelial skin tumours by two-dimensional gel electrophoresis (2-DE), densitometry and immunohistochemistry [30].
• All the K17 mutations reported here were shown to co-segregate with the disease in the pedigrees analyzed and were excluded from 100 unaffected, unrelated chromosomes by restriction enzyme analysis of K17 genomic PCR products [35].
• Immunohistochemical stainings for CK 17 will facilitate further studies on the distribution and biology of haarscheibe [36].
• CONCLUSION: Immunohistochemical detection of CK 17 and 19 seems to be a valuable additional parameter distinguishing between odontogenic keratocysts and other odontogenic--especially dentigerous--cysts which clinically are likely the most significant differential diagnoses in this context [37].

References