Expression of soybean lectin gene deletions in tobacco

1990 ◽  
Vol 11 (2) ◽  
pp. 160-167 ◽  
Author(s):  
Jon T. Lindstrom ◽  
Lila O. Vodkin ◽  
Roy W. Harding ◽  
Robert M. Goeken
Keyword(s):  
Gene Deletions ◽  
Lectin Gene ◽  
Soybean Lectin

scholarly journals An insertion sequence blocks the expression of a soybean lectin gene

Cell ◽  
1983 ◽  
Vol 33 (2) ◽  
pp. 465-475 ◽  
Author(s):  
Robert B. Goldberg ◽  
Gisela Hoschek ◽  
Lila O. Vodkin
Keyword(s):  
Insertion Sequence ◽  
Lectin Gene ◽  
Soybean Lectin

Interaction of an embryo DNA binding protein with a soybean lectin gene upstream region

Nature ◽  
1987 ◽  
Vol 328 (6132) ◽  
pp. 734-737 ◽  
Author(s):  
K. Diane Jofuku ◽  
Jack K. Okamuro ◽  
Robert B. Goldberg
Keyword(s):  
Dna Binding ◽  
Binding Protein ◽  
Dna Binding Protein ◽  
Upstream Region ◽  
Lectin Gene ◽  
Soybean Lectin

Localization of β-glucuronidase in protein bodies of transgenic tobacco seed by fusion to an amino terminal sequence of the soybean lectin gene

Plant Science ◽  
1998 ◽  
Vol 137 (2) ◽  
pp. 191-204 ◽  
Author(s):  
Reena Philip ◽  
Douglas W. Darnowski ◽  
Vijaya Sundararaman ◽  
Myeong-Je Cho ◽  
Lila O. Vodkin
Keyword(s):  
Transgenic Tobacco ◽  
Protein Bodies ◽  
Terminal Sequence ◽  
Lectin Gene ◽  
Amino Terminal ◽  
Tobacco Seed ◽  
Amino Terminal Sequence ◽  
Soybean Lectin

scholarly journals Lotus corniculatus Nodulation Specificity Is Changed by the Presence of a Soybean Lectin Gene

1998 ◽  
Vol 10 (8) ◽  
pp. 1233-1249 ◽  
Author(s):  
Pieternel van Rhijn ◽  
Robert B. Goldberg ◽  
Ann M. Hirsch
Keyword(s):  
Lotus Corniculatus ◽  
Lectin Gene ◽  
Nodulation Specificity ◽  
Soybean Lectin

Lotus corniculatus Nodulation Specificity Is Changed by the Presence of a Soybean Lectin Gene

1998 ◽  
Vol 10 (8) ◽  
pp. 1233 ◽  
Author(s):  
Pieternel van Rhijn ◽  
Robert B. Goldberg ◽  
Ann M. Hirsch
Keyword(s):  
Lotus Corniculatus ◽  
Lectin Gene ◽  
Nodulation Specificity ◽  
Soybean Lectin

Mannan-binding lectin gene polymorphisms in ulcerative colitis and Crohn's disease

2001 ◽  
Vol 120 (5) ◽  
pp. A459-A459
Author(s):  
A RECTOR ◽  
P LEMEY ◽  
W LAFFUT ◽  
E KEYAERTS ◽  
F STRUYF ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Gene Polymorphisms ◽  
Lectin Gene ◽  
Mannan Binding Lectin ◽  
Binding Lectin

Application of Two Neutral Mspl DNA Polymorphisms in the Analysis of Hereditary Protein C Deficiency

1990 ◽  
Vol 64 (02) ◽  
pp. 239-244 ◽  
Author(s):  
P H Reitsma ◽  
W te Lintel Hekkert ◽  
E Koenhen ◽  
P A van der Velden ◽  
C F Allaart ◽  
...  
Keyword(s):  
Protein C ◽  
Stop Codon ◽  
Normal Population ◽  
Amino Acid Position ◽  
Rare Allele ◽  
Dna Polymorphisms ◽  
Type I ◽  
Protein C Deficiency ◽  
Gene Deletions ◽  
Allelic Frequencies

SummaryScreening of restriction erzyme digested DNA from normal and protein C deficient individuals with a variety of probes derived from the protein C locus has revealed the existence of two neutral MspI polymorphism. One polymorphism (MI), which is located ≈7 kb upstream of the protein C gene, has allelic frequencies of 69 and 31%, and was used to exclude extensive gene deletions as a likely cause of type I protein C deficiency in 50% of cases in a panel of 22 families. Furtherrnore, the same polymorphism has been used in 5 doubly affected individuals establishing compound heterozygosity in 3 of these.The second, intragenic, polymorphism (MII) has allelic frequencies of 99 and 1% in the normal population. The frequency of the rare allele of this RFLP was with 7% much higher in a panel of 22 Dutch families with protein C deficiency. Interestingly, in all three probands that were heterozygous for MII the rare allele of MII coincided with a point mutation that leads to a stop codon in amino acid position 306 of the protein C coding sequence. This mutation may account for 14% of the protein C deficient individuals in The Netherlands.

Characterization of Partial Gene Deletions in Type III von Willebrand Disease with Alloantibody Inhibitors

1994 ◽  
Vol 72 (02) ◽  
pp. 180-185 ◽  
Author(s):  
David J Mancuso ◽  
Elodee A Tuley ◽  
Ricardo Castillo ◽  
Norma de Bosch ◽  
Pler M Mannucci ◽  
...  
Keyword(s):  
Von Willebrand Factor ◽  
Von Willebrand Disease ◽  
Pcr Analysis ◽  
Gene Deletions ◽  
Factor Gene ◽  
Type Iii ◽  
Large Deletions ◽  
Von Willebrand ◽  
Willebrand Factor

Summaryvon Willebrand factor gene deletions were characterized in four patients with severe type III von Willebrand disease and alloantibodies to von Willebrand factor. A PCR-based strategy was used to characterize the boundaries of the deletions. Identical 30 kb von Willebrand factor gene deletions which include exons 33 through 38 were identified in two siblings of one family by this method. A small 5 base pair insertion (CCTGG) was sequenced at the deletion breakpoint. PCR analysis was used to detect the deletion in three generations of the family, including two family members who are heterozygous for the deletion. In a second family, two type III vWD patients, who are distant cousins, share an -56 kb deletion of exons 22 through 43. The identification and characterization of large vWF gene deletions in these type III vWD patients provides further support for the association between large deletions in both von Willebrand factor alleles and the development of inhibitory alloantibodies.

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