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The New Mutants. Demon bear
The visionary talents of writer Chris Claremont and legendary illustrator Bill Sienkiewicz bring the Demon Bear that has haunted Danielle Moonstar's dreams to horrifying life! It took her parents, and now it has returned for Dani - and only the combined efforts of her fellow New Mutants can stop it from finishing the job! Sink your teeth into a true classic! Then, Dani's nightmare returns years later as San Francisco - and her new team X-Force, come under attack from a similarly unholy ursine!
Book
Allele-selective lowering of mutant HTT protein by HTT–LC3 linker compounds
Accumulation of mutant proteins is a major cause of many diseases (collectively called proteopathies), and lowering the level of these proteins can be useful for treatment of these diseases. We hypothesized that compounds that interact with both the autophagosome protein microtubule-associated protein 1A/1B light chain 3 (LC3)
1
and the disease-causing protein may target the latter for autophagic clearance. Mutant huntingtin protein (mHTT) contains an expanded polyglutamine (polyQ) tract and causes Huntington’s disease, an incurable neurodegenerative disorder
2
. Here, using small-molecule-microarray-based screening, we identified four compounds that interact with both LC3 and mHTT, but not with the wild-type HTT protein. Some of these compounds targeted mHTT to autophagosomes, reduced mHTT levels in an allele-selective manner, and rescued disease-relevant phenotypes in cells and in vivo in fly and mouse models of Huntington’s disease. We further show that these compounds interact with the expanded polyQ stretch and could lower the level of mutant ataxin-3 (ATXN3), another disease-causing protein with an expanded polyQ tract
3
. This study presents candidate compounds for lowering mHTT and potentially other disease-causing proteins with polyQ expansions, demonstrating the concept of lowering levels of disease-causing proteins using autophagosome-tethering compounds.
Compounds that interact with mutant huntingtin and an autophagosomal protein are able to reduce cellular levels of mutant huntingtin by targeting it for autophagic degradation, demonstrating an approach that may have potential for treating proteopathies.
Journal Article
New mutants : the complete collection
\"It's dangerous getting older. Cannonball, Dani Moonstar, Karma, Sunspot, Magma and Magik have put the band bakc together - just in time for the return of one of the most powerful threats they ever faced: Legion! Speaking of comebacks, the dead just won't stay that way as the shocking events of Necrosha hit home - and Doug Ramsey and Warlock return! As the New Mutants struggle to rediscover the strong bond they shared as teenagers, a new enemy arrives to tear them apart! The team's past returns to haunt them as they're dragged into the hellish dimension of Limbo, but will the secret they uncover there lead to the fall of the New Mutants?\" -- Page 4 of cover.
Book
SARS-CoV-2 evolution during treatment of chronic infection
The spike protein of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is critical for virus infection through the engagement of the human ACE2 protein
1
and is a major antibody target. Here we show that chronic infection with SARS-CoV-2 leads to viral evolution and reduced sensitivity to neutralizing antibodies in an immunosuppressed individual treated with convalescent plasma, by generating whole-genome ultra-deep sequences for 23 time points that span 101 days and using in vitro techniques to characterize the mutations revealed by sequencing. There was little change in the overall structure of the viral population after two courses of remdesivir during the first 57 days. However, after convalescent plasma therapy, we observed large, dynamic shifts in the viral population, with the emergence of a dominant viral strain that contained a substitution (D796H) in the S2 subunit and a deletion (ΔH69/ΔV70) in the S1 N-terminal domain of the spike protein. As passively transferred serum antibodies diminished, viruses with the escape genotype were reduced in frequency, before returning during a final, unsuccessful course of convalescent plasma treatment. In vitro, the spike double mutant bearing both ΔH69/ΔV70 and D796H conferred modestly decreased sensitivity to convalescent plasma, while maintaining infectivity levels that were similar to the wild-type virus.The spike substitution mutant D796H appeared to be the main contributor to the decreased susceptibility to neutralizing antibodies, but this mutation resulted in an infectivity defect. The spike deletion mutant ΔH69/ΔV70 had a twofold higher level of infectivity than wild-type SARS-CoV-2, possibly compensating for the reduced infectivity of the D796H mutation. These data reveal strong selection on SARS-CoV-2 during convalescent plasma therapy, which is associated with the emergence of viral variants that show evidence of reduced susceptibility to neutralizing antibodies in immunosuppressed individuals.
Chronic infection with SARS-CoV-2 leads to the emergence of viral variants that show reduced susceptibility to neutralizing antibodies in an immunosuppressed individual treated with convalescent plasma.
Journal Article
New Mutants : back to school, the complete collection
\"Dani Moonstar, Karma and Wolfsbane -- the former X-Men-in-training who helped define a generation -- are back to pass their wisdom on to the next one! But how will the New Mutants react to Professor X's up-and-coming students, who think of them as \"Old Mutants\"? Find out as a new class debuts at the Xavier School -- including Prodigy, Wallflower, Wither, Surge, Elixir, Wind Dancer and more! They may be the future of their species -- if they can survive threats like the Reavers and the hate group Purity! As the latest squad comes into its own, the originals settle into new roles as mentors -- but will Wolfsbane's desire to regain her powers cause her to cross a line?\"--Back cover.
BOOK
The new mutants. Volume 6, 1988-1989. Curse of the Valkyries
The Epic collections feature the best characters and stories from Marvel's vast history. Volumes are not published in chronological order--so start your collection today with this edition and look inside for a complete list of available and upcoming releases!
Book
Mutations of optineurin in amyotrophic lateral sclerosis
Optineurin defects in ALS
About 10% of cases of the motor neuron disease amyotrophic lateral sclerosis (ALS) are familial, but the small number of mutations so far identified account for only around 20–30% of the those cases. A new study of individuals from ALS-carrying families has now identified three different and previously unknown mutations of
OPTN
, the gene encoding optineurin.
OPTN
was earlier reported to be the causative gene of rare familial glaucoma. Optineurin's ability to inhibit activation of the regulatory protein NF-κB is lost in the mutant forms, suggesting that NF-κB inhibitors might be useful in ALS treatment.
Amyotrophic lateral sclerosis (ALS) is a disorder characterized by the degeneration of motor neurons. About 10% of cases are familial, but the mutations identified in these families account for only 20–30% of such cases. Here a new set of mutations in familial ALS is found — in the gene encoding optineurin. Given the effect of optineurin mutations on the NF-κB protein, it is suggested that inhibiting NF-κB might be useful in treating ALS.
Amyotrophic lateral sclerosis (ALS) has its onset in middle age and is a progressive disorder characterized by degeneration of motor neurons of the primary motor cortex, brainstem and spinal cord
1
. Most cases of ALS are sporadic, but about 10% are familial. Genes known to cause classic familial ALS (FALS) are superoxide dismutase 1 (
SOD1
)
2
,
ANG
encoding angiogenin
3
,
TARDP
encoding transactive response (TAR) DNA-binding protein TDP-43 (ref.
4
) and fused in sarcoma/translated in liposarcoma (
FUS
, also known as
TLS
)
5
,
6
. However, these genetic defects occur in only about 20–30% of cases of FALS, and most genes causing FALS are unknown. Here we show that there are mutations in the gene encoding optineurin (
OPTN
), earlier reported to be a causative gene of primary open-angle glaucoma (POAG)
7
, in patients with ALS. We found three types of mutation of
OPTN
: a homozygous deletion of exon 5, a homozygous Q398X nonsense mutation and a heterozygous E478G missense mutation within its ubiquitin-binding domain. Analysis of cell transfection showed that the nonsense and missense mutations of
OPTN
abolished the inhibition of activation of nuclear factor kappa B (NF-κB), and the E478G mutation revealed a cytoplasmic distribution different from that of the wild type or a POAG mutation. A case with the E478G mutation showed OPTN-immunoreactive cytoplasmic inclusions. Furthermore, TDP-43- or SOD1-positive inclusions of sporadic and
SOD1
cases of ALS were also noticeably immunolabelled by anti-OPTN antibodies. Our findings strongly suggest that OPTN is involved in the pathogenesis of ALS. They also indicate that NF-κB inhibitors could be used to treat ALS and that transgenic mice bearing various mutations of
OPTN
will be relevant in developing new drugs for this disorder.
Journal Article
