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101.
102.
Zusammenfassung Die mutagene Wirkung von Aethylenmethansulfonat inDrosophila-Männchen wird durch DMSO um 46% erhöht. DMSO allein kann keine Mutation über die Spontanrate hinaus induzieren. 相似文献
103.
S. S. Sharma 《Cellular and molecular life sciences : CMLS》1985,41(1):45-46
Summary Mercuric acetate, at 5.0×10–5 M, stimulates the mobilization of total nitrogen and phosphate reserves from cotyledons during seedling growth inCicer arietinum cv H208 whereas it suppresses the same process at 2.5×10–4 M.Thanks are due to Dr D. Banerji for providing facilities and helpful suggestions. 相似文献
104.
105.
J M Sharma 《Nature》1974,247(436):117-118
106.
Many lines of evidence indicate that genetically distinct subtypes of motor neurons are specified during development, with each type having characteristic properties of axon guidance and cell-body migration. Motor neuron subtypes express unique combinations of LIM-type homeodomain factors that may act as intrinsic genetic regulators of the cytoskeletal events that mediate cell migration, axon navigation or both. Although experimentally displaced motor neurons can pioneer new routes to their targets, in many cases the axons of motor neurons in complete isolation from their normal territories passively follow stereotypical pathways dictated by the environment. To investigate the nonspecific versus genetically controlled regulation of motor connectivity we forced all motor neurons to express ectopically a LIM gene combination appropriate for the subgroup that innervates axial muscles. Here we show that this genetic alteration is sufficient to convert the cell body settling pattern, gene-expression profile and axonal projections of all motor neurons to that of the axial subclass. Nevertheless, elevated occupancy of the axial pathway can override their genetic program, causing some axons to project to alternative targets. 相似文献
107.
Vanesa Lafarga Olga Tapia Sahil Sharma Rocio Bengoechea Georg Stoecklin Miguel Lafarga Maria T. Berciano 《Cellular and molecular life sciences : CMLS》2018,75(3):527-546
The survival of motor neuron (SMN) protein plays an essential role in the biogenesis of spliceosomal snRNPs and the molecular assembly of Cajal bodies (CBs). Deletion of or mutations in the SMN1 gene cause spinal muscular atrophy (SMA) with degeneration and loss of motor neurons. Reduced SMN levels in SMA lead to deficient snRNP biogenesis with consequent splicing pathology. Here, we demonstrate that SMN is a novel and specific target of the acetyltransferase CBP (CREB-binding protein). Furthermore, we identify lysine (K) 119 as the main acetylation site in SMN. Importantly, SMN acetylation enhances its cytoplasmic localization, causes depletion of CBs, and reduces the accumulation of snRNPs in nuclear speckles. In contrast, the acetylation-deficient SMNK119R mutant promotes formation of CBs and a novel category of promyelocytic leukemia (PML) bodies enriched in this protein. Acetylation increases the half-life of SMN protein, reduces its cytoplasmic diffusion rate and modifies its interactome. Hence, SMN acetylation leads to its dysfunction, which explains the ineffectiveness of HDAC (histone deacetylases) inhibitors in SMA therapy despite their potential to increase SMN levels. 相似文献
108.
Witt H Sahin-Tóth M Landt O Chen JM Kähne T Drenth JP Kukor Z Szepessy E Halangk W Dahm S Rohde K Schulz HU Le Maréchal C Akar N Ammann RW Truninger K Bargetzi M Bhatia E Castellani C Cavestro GM Cerny M Destro-Bisol G Spedini G Eiberg H Jansen JB Koudova M Rausova E Macek M Malats N Real FX Menzel HJ Moral P Galavotti R Pignatti PF Rickards O Spicak J Zarnescu NO Böck W Gress TM Friess H Ockenga J Schmidt H Pfützer R Löhr M Simon P Weiss FU Lerch MM Teich N Keim V Berg T Wiedenmann B Luck W 《Nature genetics》2006,38(6):668-673
Chronic pancreatitis is a common inflammatory disease of the pancreas. Mutations in the genes encoding cationic trypsinogen (PRSS1) and the pancreatic secretory trypsin inhibitor (SPINK1) are associated with chronic pancreatitis. Because increased proteolytic activity owing to mutated PRSS1 enhances the risk for chronic pancreatitis, mutations in the gene encoding anionic trypsinogen (PRSS2) may also predispose to disease. Here we analyzed PRSS2 in individuals with chronic pancreatitis and controls and found, to our surprise, that a variant of codon 191 (G191R) is overrepresented in control subjects: G191R was present in 220/6,459 (3.4%) controls but in only 32/2,466 (1.3%) affected individuals (odds ratio 0.37; P = 1.1 x 10(-8)). Upon activation by enterokinase or trypsin, purified recombinant G191R protein showed a complete loss of trypsin activity owing to the introduction of a new tryptic cleavage site that renders the enzyme hypersensitive to autocatalytic proteolysis. In conclusion, the G191R variant of PRSS2 mitigates intrapancreatic trypsin activity and thereby protects against chronic pancreatitis. 相似文献
109.
Xiao H Han B Lodyga M Bai XH Wang Y Liu M 《Cellular and molecular life sciences : CMLS》2012,69(7):1137-1151
Actin filament-associated protein (AFAP) plays a critical role in the regulation of actin filament integrity, formation and
maintenance of the actin network, function of focal contacts, and cell migration. Here, we show that endogenous AFAP was present
not only in the cytoskeletal but also in the cytosolic fraction. Depolymerization of actin filaments with cytochalasin D or
latrunculin A increased AFAP in the cytosolic fraction. AFAP harbors an actin-binding domain (ABD) in its C-terminus. AFAPΔABD,
an AFAP mutant with selective ABD deletion, was mainly in the cytosolic fraction when overexpressed in the cells, which was
associated with a disorganized cytoskeleton with reduced stress fibers, accumulation of F-actin on cellular membrane, and
formation of actin-rich small dots. Cortactin, a well-known podosome marker, was colocalized with AFAPΔABD in these small
dots at the ventral surface of the cell, indicating that these small dots fulfill certain criteria of podosomes. However,
these podosome-like small dots did not digest gelatin matrix. This may be due to the reduced interaction between AFAPΔABD
and c-Src. When AFAPΔABD-transfected cells were stimulated with phorbol ester, they formed podosome-like structures with larger
sizes, less numerous and longer life span, in comparison with wild-type AFAP-transfected cells. These results indicate that
the association of AFAP with F-actin through ABD is crucial for AFAP to regulate cytoskeletal structures. The AFAPΔABD, as
cytosolic proteins, may be more accessible to the cellular membrane, podosome-like structures, and thus be more interactive
for the regulation of cellular functions. 相似文献
110.
Mi W Pawlik M Sastre M Jung SS Radvinsky DS Klein AM Sommer J Schmidt SD Nixon RA Mathews PM Levy E 《Nature genetics》2007,39(12):1440-1442
Using transgenic mice expressing human cystatin C (encoded by CST3), we show that cystatin C binds soluble amyloid-beta peptide and inhibits cerebral amyloid deposition in amyloid-beta precursor protein (APP) transgenic mice. Cystatin C expression twice that of the endogenous mouse cystatin C was sufficient to substantially diminish amyloid-beta deposition. Thus, cystatin C has a protective role in Alzheimer's disease pathogenesis, and modulation of cystatin C concentrations may have therapeutic implications for the disease. 相似文献