In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.

Input: Consider Input: Background: We present here the recent update of AMS algorithm for identification of post-translational modification (PTM) sites in proteins based only on sequence information, using artificial neural network (ANN) method. The query protein sequence is dissected into overlapping short sequence segments. Ten different physicochemical features describe each amino acid; therefore nine residues long segment is represented as a point in a 90 dimensional space. The database of sequence segments with confirmed by experiments post-translational modification sites are used for training a set of ANNs. The efficiency of the classification for each type of modification and the prediction power of the method is estimated here using recall (sensitivity), precision values, the area under receiver operating characteristic (ROC) curves and leave-one-out tests (LOOCV). The significant differences in the performance for differently optimized neural networks are observed, yet the AMS 3.0 tool integrates those heterogeneous classification schemes into the single consensus scheme, and it is able to boost the precision and recall values independent of a PTM type in comparison with the currently available state-of-the art methods. The standalone version of AMS 3.0 presents an efficient way to indentify post-translational modifications for whole proteomes. The training datasets, precompiled binaries for AMS 3.0 tool and the source code are available at Additional file 1 Supplementary materials for the publication. Supplementary.xls contains detailed results of training and testing of AMS 3.0 tool in MS Excel file format. Additional file 2 PTM predictor software with training data. PTM_Archive.tar.gz includes the predictor software binaries together with all trained ANNs in tar.gz compressed form.

Output: AMS 3.0: prediction of post-translational modifications

Input: Consider Input: Four Massachusetts-type (Mass-type) strains of infectious bronchitis coronavirus (IBV) were compared genetically with the pathogenic M41 and H120 vaccine strains using the complete genomic sequences. The results revealed that strains ck/CH/LNM/091017 and ck/CH/LDL/101212 were closely related to the H120 vaccine, which suggests that they might represent re-isolations of vaccine strains or variants of vaccine strains that have resulted from the accumulated point mutations after several passages in chickens. In contrast, strains ck/CH/LHLJ/07VII and ck/CH/LHLJ/100902 had a close genetic relationship with the pathogenic M41 strain. In addition, molecular markers have been identified that distinguish between field and vaccine (or vaccine-like) Mass-type viruses, which may be able to differentiate between field and vaccine strains for diagnostic purposes. Phylogenetic analysis, and pairwise comparison of full-length genomes and the nine genes, identified the occurrence of recombination events in the genome of strain CK/VH/LHLJ/07VII, which suggests that this virus originated from recombination events between M41-and H120-like strains at the switch site located at the 3 0 end of the nucleocapsid (N) genes. To our knowledge, this is the first time that evidence for the evolution and natural recombination under field conditions between Mass-type pathogenic and vaccinal IBV strains has been documented. These findings provide insights into the emergence and evolution of the Mass-type IB coronaviruses and may help to explain the emergence of Mass-type IBV in chicken flocks all over the world.

Output: Comparative analysis of four Massachusetts type infectious bronchitis coronavirus genomes reveals a novel Massachusetts type strain and evidence of natural recombination in the genome

Input: Consider Input: Background: The HIV-1 RNA genome has a biased nucleotide composition with a surplus of As. Several hypotheses have been put forward to explain this striking phenomenon, but the A-count of the HIV-1 genome has thus far not been systematically manipulated. The reason for this reservation is the likelihood that known and unknown sequence motifs will be affected by such a massive mutational approach, thus resulting in replication-impaired virus mutants. We present the first attempt to increase and decrease the A-count in a relatively small polymerase (pol) gene segment of HIV-1 RNA. To minimize the mutational impact, a new mutational approach was developed that is inspired by natural sequence variation as present in HIV-1 isolates. This phylogeny-instructed mutagenesis allowed us to create replication-competent HIV-1 mutants with a significantly increased or decreased local A-count. The local A-count of the wild-type (wt) virus (40.2%) was further increased to 46.9% or reduced to 31.7 and 26.3%. These HIV-1 variants replicate efficiently in vitro, despite the fact that the pol changes cause a quite profound move in HIV-SIV sequence space. Extrapolating these results to the complete 9 kb RNA genome, we may cautiously suggest that the A-rich signature does not have to be maintained. This survey also provided clues that silent codon changes, in particular from G-to-A, determine the subtype-specific sequence signatures.
Output: HIV-1 tolerates changes in A-count in a small segment of the pol gene