scholarly journals Biochemical studies of toxic agents. 4. A study of ethereal sulphate formation in vivo using radioactive sulphur

1953 ◽  
Vol 54 (1) ◽  
pp. 142-148 ◽  
Author(s):  
J. C. Laidlaw ◽  
L. Young
2000 ◽  
Vol 113 (16) ◽  
pp. 2821-2827 ◽  
Author(s):  
L. Quarmby

Recent biochemical studies of the AAA ATPase, katanin, provide a foundation for understanding how microtubules might be severed along their length. These in vitro studies are complemented by a series of recent reports of direct in vivo observation of microtubule breakage, which indicate that the in vitro phenomenon of catalysed microtubule severing is likely to be physiological. There is also new evidence that microtubule severing by katanin is important for the production of non-centrosomal microtubules in cells such as neurons and epithelial cells. Although it has been difficult to establish the role of katanin in mitosis, new genetic evidence indicates that a katanin-like protein, MEI-1, plays an essential role in meiosis in C. elegans. Finally, new proteins involved in the severing of axonemal microtubules have been discovered in the deflagellation system of Chlamydomonas.


1997 ◽  
Vol 41 (5) ◽  
pp. 666-673 ◽  
Author(s):  
Terttu Suormala ◽  
Brian Fowler ◽  
Marinus Duran ◽  
Alain Burtscher ◽  
Arno Fuchshuber ◽  
...  

2018 ◽  
Vol 115 (33) ◽  
pp. E7748-E7757 ◽  
Author(s):  
Rami Khoriaty ◽  
Geoffrey G. Hesketh ◽  
Amélie Bernard ◽  
Angela C. Weyand ◽  
Dattatreya Mellacheruvu ◽  
...  

Approximately one-third of the mammalian proteome is transported from the endoplasmic reticulum-to-Golgi via COPII-coated vesicles. SEC23, a core component of coat protein-complex II (COPII), is encoded by two paralogous genes in vertebrates (Sec23a and Sec23b). In humans, SEC23B deficiency results in congenital dyserythropoietic anemia type-II (CDAII), while SEC23A deficiency results in a skeletal phenotype (with normal red blood cells). These distinct clinical disorders, together with previous biochemical studies, suggest unique functions for SEC23A and SEC23B. Here we show indistinguishable intracellular protein interactomes for human SEC23A and SEC23B, complementation of yeast Sec23 by both human and murine SEC23A/B, and rescue of the lethality of sec23b deficiency in zebrafish by a sec23a-expressing transgene. We next demonstrate that a Sec23a coding sequence inserted into the murine Sec23b locus completely rescues the lethal SEC23B-deficient pancreatic phenotype. We show that SEC23B is the predominantly expressed paralog in human bone marrow, but not in the mouse, with the reciprocal pattern observed in the pancreas. Taken together, these data demonstrate an equivalent function for SEC23A/B, with evolutionary shifts in the transcription program likely accounting for the distinct phenotypes of SEC23A/B deficiency within and across species, a paradigm potentially applicable to other sets of paralogous genes. These findings also suggest that enhanced erythroid expression of the normal SEC23A gene could offer an effective therapeutic approach for CDAII patients.


1962 ◽  
Vol 82 (3) ◽  
pp. 457-466 ◽  
Author(s):  
RP HOPKINS ◽  
CJW BROOKS ◽  
L YOUNG

1964 ◽  
Vol 90 (3) ◽  
pp. 588-596 ◽  
Author(s):  
EA Barnsley ◽  
AER Thomson ◽  
L Young

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