Changes in Reelin levels as well as Reelin signaling alter cognitive function. This can be accomplished by administering a therapeutically effective amount of a repeat fragment of Reelin, or a construct formed from fragment repeats of Reelin to a patient or subject. Changes to Reelin levels can be used to treat various neurodegenerative diseases, neuronal insults, or stroke, such as fragile X syndrome, William's syndrome, Rett syndrome, Down's syndrome, Angelman syndrome, autism, ischemia, hypoxia, Alzheimer's disease, and schizophrenia. Reelin can also be used to alter dendritic spine density, diminished long-term potentiation, and diminished synaptic plasticity and associative learning deficits. Constructs formed from repeat region 3 of full length Reelin and repeat region 5 of full length Reelin, or repeat region 3 of full length Reelin and repeat region 6 of full length Reelin have been found particularly useful.

Methods of using a separation media to isolate a target molecule that includes a carbohydrate are disclosed. The separation media includes a support substrate and a plurality of separation ligands immobilized on the support substrate. The plurality of separation ligands include an affinity capable of recognizing and binding to a carbohydrate.

The present invention is directed to a recombinant herpesvirus comprising a heterologous polypeptide ligand capable of binding to a target molecule and fused to or inserted into glycoprotein B at specific sites. The herpesvirus may comprise more than one ligand, and the additional ligand(s) may be comprised by a modified glycoprotein D and/or modified glycoprotein H. This allows the herpesvirus to target a cell for therapeutic purposes, and a cell for virus production. The present invention further comprises a pharmaceutical composition comprising the herpesvirus, the herpesvirus for use in the treatment of a tumor, infection, degenerative disorder or senescence-associated disease, a nucleic acid and a vector coding for the gB, a polypeptide comprising the gB, and a cell comprising the herpesvirus, nucleic acid, vector or polypeptide. Moreover, a method for infecting a cell with the herpesvirus or for producing the herpesvirus is disclosed.

Provided is a method for measuring a glycoprotein using an enzymatic method, and the method includes simplified steps.

Provided is a reagent that is suitable for measurement of a glycoprotein and contains a compound capable of stabilizing a leuco dye.

The invention provides a prophylactic agent or therapeutic agent for fibrodysplasia ossificans progressiva, containing as an active ingredient a binding inhibitor that inhibits interaction between activin and activin A receptor type I (ACVR1), or an expression suppressor that suppresses expression of activin.

In certain aspects, the disclosure relates to a recombinant nucleic acid molecule (e.g. RNA molecule) encoding one or more polypeptides selected from the group consisting of chitinase-3-like protein 1 (CHI3L1), a fibroblast growth factor (FGF), interleukin-2 ORF7 (IL-2 ORF7), interleukin-2 (IL-2), an interleukin-17 (IL-17) protein, and an IL-17 receptor, wherein the recombinant RNA molecule comprises at least one chemical modification. Cells, pharmaceutical compositions and wound dressings comprising one or more of the recombinant nucleic acid molecules are also disclosed. Methods of promoting wound healing in a subject are further disclosed.

A method for establishing eukaryotic expression cell line of CD36 mutant gene that encodes CD36 deficiency, the method including: (1) extracting total RNA from a whole blood sample derived from a CD36-deficient individual, and amplifying a coding sequence (CDS) in CD36 mRNA, to obtain a cDNA sequence fragment of the mutant CD36 gene; (2) splicing and amplifying the mutant CD36 gene and the EGFP fluorescent gene by SOE-PCR (Gene Splicing By Overlap Extension PCR) using four forward and reverse primers, to obtain a mutant gene fragment of MT-CD36-EGFP; (3) constructing and amplifying a MT-CD36-EGFP-pLV4/StripII-HIS10 eukaryotic expression vector including the mutant CD36 gene and the EGFP fluorescent gene; (4) transfecting the MT-CD36-EGFP-pLV4/StripII-HIS10 eukaryotic expression vector into the CHO-K1 cell line by using virus-mediated transfection of eukaryotic cells.

Methods and devices are described for using a controlled extensional strain to organize prefibrillar collagen and/or elastin solutions into an organized array of fibrils. The organized array of collagen fibrils produced by the disclosed methods and devices can be used for tissue engineering applications.

Evolved sortases exhibiting enhanced reaction kinetics and/or altered substrate preferences are provided herein, for example evolved sortases that bind recognitions motifs comprising a LAXT or LPXS sequence. Also provided are methods (e.g., orthogonal transpeptidation and diagnostics methods) for using such sortases. Kits comprising materials, reagents, and cells for carrying out the methods described herein are also provided.