In this task, you are given a abstract of article and corresponding title of an article. Your task is to generate label "yes" if title is right for article, otherwise generate "no".

Ex Input:
Abstract: UNLABELLED Morphological characteristics of dendritic spines form the basis of cognitive ability. However, molecular mechanisms involved in fine-tuning of spine morphology during development are not fully understood. Moreover, it is unclear whether, and to what extent, these developmental mechanisms determine the normal adult spine morphological features. Here, we provide evidence that 2-isoform of Rac-specific GTPase-activating protein -chimaerin (2-chimaerin) is involved in spine morphological refinement during late postnatal period, and furthermore show that this developmental 2-chimaerin function affects adult spine morphologies. We used a series of mice with global and conditional knock-out of -chimaerin isoforms (1-chimaerin and 2-chimaerin). 2-Chimaerin disruption, but not 1-chimaerin disruption, in the mouse results in an increased size (and density) of spines in the hippocampus. In contrast, overexpression of 2-chimaerin in developing hippocampal neurons induces a decrease of spine size. Disruption of 2-chimaerin suppressed EphA-mediated spine morphogenesis in cultured developing hippocampal neurons. 2-Chimaerin disruption that begins during the juvenile stage results in an increased size of spines in the hippocampus. Meanwhile, spine morphologies are unaltered when 2-chimaerin is deleted only in adulthood. Consistent with these spine morphological results, disruption of 2-chimaerin beginning in the juvenile stage led to an increase in contextual fear learning in adulthood; whereas contextual learning was recently shown to be unaffected when 2-chimaerin was deleted only in adulthood. Together, these results suggest that 2-chimaerin signaling in developmental stages contributes to determination of the morphological features of adult spines and establishment of normal cognitive ability. SIGNIFICANCE STATEMENT Recent studies of neurodevelopmental disorders in humans and their animal models have led to an attractive hypothesis that spine morphogenesis during development forms the basis of adult cognition. In particular, the roles of Rac and its regulators, such as Rac-specific GTPase-activating proteins (RacGAPs) and Rac guanine nucleotide exchange factors, are a topic of focus in spine morphogenesis and cognitive ability. Using a series of mice with global and conditional knock-out (KO) of RacGAP -chimaerin isoforms (1-chimaerin and 2-chimaerin), we provide compelling evidence demonstrating that 2-chimaerin is involved in spine morphological refinement during late postnatal development and that this developmental 2-chimaerin function affects adult spine morphologies. Furthermore, our results clearly showed that 2-chimaerin signaling during late postnatal development contributes to normal cognitive ability in adult mice.. Title: DNA damage and Repair Modify DNA methylation and Chromatin Domain of the Targeted Locus: Mechanism of allele methylation polymorphism

Ex Output:
no

Ex Input:
Abstract: The packaging of the eukaryotic genome in chromatin presents barriers that restrict the access of enzymes that process DNA. To overcome these barriers, cells possess a number of multi-protein, ATP-dependent chromatin remodelling complexes, each containing an ATPase subunit from the SNF2/SWI2 superfamily. Chromatin remodelling complexes function by increasing nucleosome mobility and are clearly implicated in transcription. Here we have analysed SNF2/SWI2- and ISWI-related proteins to identify remodelling complexes that potentially assist other DNA transactions. We purified a complex from Saccharomyces cerevisiae that contains the Ino80 ATPase. The INO80 complex contains about 12 polypeptides including two proteins related to the bacterial RuvB DNA helicase, which catalyses branch migration of Holliday junctions. The purified complex remodels chromatin, facilitates transcription in vitro and displays 3' to 5' DNA helicase activity. Mutants of ino80 show hypersensitivity to agents that cause DNA damage, in addition to defects in transcription. These results indicate that chromatin remodelling driven by the Ino80 ATPase may be connected to transcription as well as DNA damage repair.. Title: THE ORIGIN AND DIFFERENTIATION OF MICROGLIAL CELLS DURING DEVELOPMENT

Ex Output:
no

Ex Input:
Abstract: The cyclin-dependent kinase Cdk2 associates with cyclins A, D, and E and has been implicated in the control of the G1 to S phase transition in mammals. To identify potential Cdk2 regulators, we have employed an improved two-hybrid system to isolate human genes encoding Cdk-interacting proteins (Cips). CIP1 encodes a novel 21 kd protein that is found in cyclin A, cyclin D1, cyclin E, and Cdk2 immunoprecipitates. p21CIP1 is a potent, tight-binding inhibitor of Cdks and can inhibit the phosphorylation of Rb by cyclin A-Cdk2, cyclin E-Cdk2, cyclin D1-Cdk4, and cyclin D2-Cdk4 complexes. Cotransfection experiments indicate that CIP1 and SV40 T antigen function in a mutually antagonistic manner to control cell cycle progression.. Title: The p21 Cdk-interacting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases.

Ex Output:
yes