| Original language | English (US) |
|---|---|
| Pages (from-to) | 397-400 |
| Number of pages | 4 |
| Journal | Progress in clinical and biological research |
| Volume | 217 B |
| State | Published - 1986 |
ASJC Scopus subject areas
- General Medicine
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In: Progress in clinical and biological research, Vol. 217 B, 1986, p. 397-400.
Research output: Contribution to journal › Article › peer-review
}
TY - JOUR
T1 - The structure of short-chain collagen genes.
AU - Lozano, G.
AU - Ninomiya, Y.
AU - Olsen, B. R.
N1 - Funding Information: THE STRUCTURE OF SHORT-CHAIN COLLAGEN GENES. G. Lozano, Y. Ninomi~a and B.R.Olsen. Department of Biochemistry, UMDNJ-Rutgers Medical School, Piscataway, N.J. 08854. We have recently characterized two cDNAs, pYN1738 and pYN1731, that code for novel and unusual short-chain collagens. To study the structure and developmental regulation of the corresponding genes, we have isolated genomic clones from chicken libraries. Based on restriction endonuclease mapping and nucleotide sequencing of the clones, we conclude that short-chain collagen genes are small and have an exon-intron structure different from that of interstitial collagen genes. Based on these results we propose that vertebrates contain at least two classes of collagen genes: Class A genes code for interstitial collagens. They contain multiple small exons (h5,54,99, 108 bp) encoding a long triple-helical domain. Class B genes code for short collagenous polypeptides with several triple-helical domains. Their exons have lengths that are different from those of Class A genes. (Supported by NIH grants AM 21471 and AM 34059). Funding Information: EPITHELIAL-MESENCH~IAL INTERACTIONS REGULATE AMELOGENIN GENE EXPRESSION. M.L. Snead,M.Zeichner-David,E.Lau,P.Bringas, Jr.,J.Vides,C.Bessem,M.MacDougall,V. Santos,and H.C.Slavkin. Univ. of So. Calif., Craniofacial Biology, University Park MC0191, Los Angeles, Calif. 90089-0191. Tooth organ morphogenesis and cytodifferentiation is mediated by reciprocal epithelial-mesenchymal interactions. Expression of the major mouse enamel matrix constituent amelogenin is limited to ameloblasts, whose differentiation is dependent on signals originating in neu-rocrest derived ectomesenchyme. We are interested in determining when and how these signals operate. Cytoplasmic RNA from molar organs (cap through crown)were analyzed by hybridization to a cloned amelogenin cDNA. Amelogenin-encoding RNA was first detected at Theiler stage 27. Amelogenin proteins were immunodetected from organs of comparable developmental stages maintained in serumless, chemically-defined media. Neither instructive signal nor the epithelial response is strictly dependent on serum factors. Supported by NIH Grant No. DE 06425 and DE 02848.
PY - 1986
Y1 - 1986
UR - http://www.scopus.com/inward/record.url?scp=0022511148&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0022511148&partnerID=8YFLogxK
M3 - Article
C2 - 3755828
AN - SCOPUS:0022511148
SN - 0361-7742
VL - 217 B
SP - 397
EP - 400
JO - Progress in clinical and biological research
JF - Progress in clinical and biological research
ER -