Я короче сделал, только для крутых я тока учусь сори
A fanart of one of the character from the Risk of Rain 2, namely - the Huntress. I was trying to apply different (but rather similar) cartoonish styles with some variations in linework, shading and details as a some kind of training routine. I personally
All RoR characters on hama! Risk of rain
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Fan art of the Clay Dunestrider from Risk of Rain 2.
Charles Darwin was obsessed with domestic pigeons. He thought they held the secrets of selection in their beaks. Free from the bonds of natural selection, the 350-plus breeds of domestic pigeons have beaks of all shapes and sizes within a single species (Columba livia). The most striking are beaks so short that they sometimes prevent parents from feeding their own young. Centuries of interbreeding taught early pigeon fanciers that beak length was likely regulated by just a few heritable factors. Yet modern geneticists have failed to solve Darwin's mystery by pinpointing the molecular machinery controlling short beaks—until now.
On this day, 7 May 1983 … Credit where it’s due to Roy of the Rovers – for a comic that was in some ways repetitive and formulaic, it did know how to play its audience and produced quite a few iconic covers over the years. If Roy Race wasn’t being shot, dismembered, married or divorced, or losing
The season of 1983-84 feels to me like one of Roy of the Rovers’ longest years yet, although no less dramatic for that. The strip was extended to four pages long for most weeks during this time: Roy occupied the front cover of the comic most weeks, then continued on his usual double-page spread in
GCD :: Cover :: Tiger #6 February 1960 [276]
For a generation of football fans, the names Melchester Rovers and Roy Race conjure up dozens of happy childhood memories and now the famous comic strip is being brought into the 21st century as an iPad archive.
My third attempt on makin some comic! I got heavily back in ror2 and dead cells and noticed there was a coliding between those, so i made a small comic for fun :) I KEEP FORGETTING THIS APP EXISTS... Ill try to not forget to post all the things i do/did...
The ER is hub for protein folding. Proteins that harbor a Frizzled cysteine-rich domain (FZ-CRD) possess 10 conserved cysteine motifs held by a unique disulfide bridge pattern which attains a correct fold in the ER. Little is known about implications of disease-causing missense mutations within FZ-CRD families. Mutations in FZ-CRD of Frizzled class receptor 4 (FZD4) and Muscle, skeletal, receptor tyrosine kinase (MuSK) and Receptor tyrosine kinase-like orphan receptor 2 (ROR2) cause Familial Exudative Vitreoretinopathy (FEVR), Congenital Myasthenic Syndrome (CMS), and Robinow Syndrome (RS) respectively. We highlight reported pathogenic inherited missense mutations in FZ-CRD of FZD4, MuSK and ROR2 which misfold, and traffic abnormally in the ER, with ER-associated degradation (ERAD) as a common pathogenic mechanism for disease. Our review shows that all studied FZ-CRD mutants of RS, FEVR and CMS result in misfolded proteins and/or partially misfolded proteins with an ERAD fate, thus we coin them as “disorders of FZ-CRD”. Abnormal trafficking was demonstrated in 17 of 29 mutants studied; 16 mutants were within and/or surrounding the FZ-CRD with two mutants distant from FZ-CRD. These ER-retained mutants were improperly N-glycosylated confirming ER-localization. FZD4 and MuSK mutants were tagged with polyubiquitin chains confirming targeting for proteasomal degradation. Investigating the cellular and molecular mechanisms of these mutations is important since misfolded protein and ER-targeted therapies are in development. The P344R-MuSK kinase mutant showed around 50% of its in-vitro autophosphorylation activity and P344R-MuSK increased two-fold on proteasome inhibition. M105T-FZD4, C204Y-FZD4, and P344R-MuSK mutants are thermosensitive and therefore, might benefit from extending the investigation to a larger number of chemical chaperones and/or proteasome inhibitors. Nonetheless, FZ-CRD ER-lipidation it less characterized in the literature and recent structural data sheds light on the importance of lipidation in protein glycosylation, proper folding, and ER trafficking. Current treatment strategies in-place for the conformational disease landscape is highlighted. From this review, we envision that disorders of FZ-CRD might be receptive to therapies that target FZ-CRD misfolding, regulation of fatty acids, and/or ER therapies; thus paving the way for a newly explored paradigm to treat different diseases with common defects.
