CP Poly(A) RNA Binding Immunity via Outside-in Glycosyltransfer with MT of BTRC-Activating L12535 and PIN1 Subnetworks for Cognition in PFC|CD14

Background: Ras suppressor protein 1 (L12535) and peptidylprolyl cis/trans isomerase NIMA-interacting 1 (PIN1) common molecular and knowledge subnetworks containing microtubule associated protein 1B-MAP1B_1 (upstream) related to cognition by references were identied in human left hemisphere, based on our established signicant high expression beta-transducin repeat containing E3 ubiquitin protein ligase (BTRC)-activating downstream Gene (protein) reconstruction network inference (GRNInfer) and Database for Annotation, Visualization and Integrated Discovery (DAVID). Results: Our results show the common molecules exostosin-like glycosyltransferase 2 (EXTL2) interaction with MAP1B_1 both activating TERF1_1 with HSP90AB1 from BTRC-activating downstream GRNInfer database; The common biological process and molecular function of MAP1B_1, TERF1_1 as microtubule (MT) binding; HSP90AB1 as poly(A) RNA binding; BTRC, HSP90AB1, PIN1 as innate immune response from BTRC-activating downstream DAVID database; The common cellular component of EXTL2 at integral component of membrane; MAP1B_1, HSP90AB1, TERF1_1 at cytoplasm (CP); The common tissue distributions of L12535 and PIN1 in Prefrontal Cortex (PFC), PB cluster of differentiation (CD)14+Monocytes. Conclusions: We propose and mutual positively verify CP poly(A) RNA binding immunity via outside-in glycosyltransfer with MT of BTRC-activating L12535 and PIN1 subnetworks for cognition in PFC|CD14.


Background
Microtubule associated protein 1B (MAP1B_1) is not only the more active molecule of our established high beta-transducin repeat containing E3 ubiquitin protein ligase (BTRC)-activating downstream network, but also the common molecule of Ras suppressor protein 1 (L12535) and peptidylprolyl cis/trans isomerase NIMA-interacting 1 (PIN1) subnetworks in human left hemisphere from our established high BTRC-activating downstream network. MAP1B_1, L12535 and PIN1 or the related family molecules have been previously published associations with cognition in the references. Such as, adenosine A2A receptor inactivation alleviates early-onset cognitive dysfunction after traumatic brain injury involving an inhibition of tau hyperphosphorylation [1].
Cotinine improves visual recognition memory and decreases cortical Tau phosphorylation in the Tg6799 mice [2]. RAS modulation prevents progressive cognitive impairment after experimental stroke as a randomized, blinded preclinical trial [3]. RAS inhibition attenuates cognitive impairment via reducing blood-brain barrier permeability in hypertensive subjects [4]. Activity-dependent isomerization of Kv4.2 by Pin1 regulates cognitive exibility [5]. PIN-1 promoter polymorphisms in mild cognitive impairment and susceptibility to Alzheimer's disease as a preliminary report [6]. However, L12535 and PIN1 subnetworks containing MAP1B_1 (upstream) has not been explored for the novel molecular and cellular mechanisms of cognition from high BTRC-activating downstream network.
In the paper, L12535 and PIN1 feedback/up/downstream molecular subnetworks from our established signi cant high expression BTRC-activating downstream Gene (protein) reconstruction network inference (GRNInfer) [7] database will be constructed in human left hemisphere successively by signi cance analysis of microarrays (SAM) (fold change ≥ 2), Pearson positive correlation coe cient (CC ≥ 0.25) database with BTRC, other mutual positive Pearson correlation (CC ≥ 0.25), respectively. L12535 and PIN1 common molecular subnetworks containing MAP1B_1 (upstream) will be computed from high BTRC-activating downstream GRNInfer database. L12535 and PIN1 common biological process, molecular function, cellular component subnetworks containing MAP1B_1 (upstream) will be computed from high BTRC-activating downstream Database for Annotation, Visualization and Integrated Discovery (DAVID) GOTERM_BP_DIRECT, GOTERM_MF_DIRECT, GOTERM_CC_DIRECT [8,9]. L12535 and PIN1 common and different tissue distributions will be calculated from high BTRC-activating downstream DAVID GNF_U133A_QUARTILE and UNIGENE_EST_QUARTILE database.
Methods 441 signi cant high expression molecules in 14 human left hemisphere were identi ed based on 12,558 genes compared with the corresponding low expression of 15 chimpanzee left hemispheres in GDS2678 [16] (public free from NCBI) by SAM [17] (http://www-stat.stanford.edu/~tibs/SAM/), including the brain cerebrum, anterior cingulate cortex, anterior inferior parietal cortex, anterior inferior temporal cortex, middle frontal gyrus, the frontal pole, etc. Data were processed using a log base of two and two unpaired classes with minimum fold change (≥ 2). A false-discovery rate of 0% was chosen. Low BTRC-activating downstream knowledge network was identi ed in chimpanzee left hemisphere from our established signi cant low expression BTRC activation DAVID database (https://david.ncifcrf.gov/). Low BTRC-activating downstream common biological process, molecular function, cellular component    decline [10]. Microstructural changes in the brain mediate the association of HSPB2 with cognitive decline [11]. TERF1 and TERF2 downregulate telomere length in cognitive de cit at the late period after low-dose exposure [12]. Low BTRC-activating downstream molecular network and the related family members have been reported relationship with cognition including ENPP2_2, MED6, NPC1, RCBTB2, WDR57 in the references. Such as, cognitive de cits associated with a high-fat diet and insulin resistance are enhanced by overexpression of ecto-nucleotide pyrophosphatase phosphodiesterase-1 [13]. Psychiatric and cognitive symptoms associated with niemann-pick type C Disease [14]. Role of Wdr45b in maintaining cognitive function [15].
Our results show the common molecules exostosin-like glycosyltransferase 2 (EXTL2) interaction with MAP1B_1 both activating TERF1_1 with HSP90AB1; The common biological process and molecular function of MAP1B_1, TERF1_1 as microtubule (MT) binding; HSP90AB1 as poly(A) RNA binding; BTRC, HSP90AB1, PIN1 as innate immune response in human left hemisphere from our established high BTRCactivating downstream GRNInfer, DAVID GOTERM_BP_DIRECT and GOTERM_MF_DIRECT database ( Fig. 1-2

Conclusion
We put forward and mutual positively verify CP poly(A) RNA binding immunity via outside-in glycosyltransfer with MT of BTRC-activating L12535 and PIN1 subnetworks for cognition in PFC|CD14, and also negatively verify our hypothesis in low BTRC-activating downstream network of chimpanzee left hemisphere. Other BTRC-activating downstream molecular and knowledge subnetworks containing MAP1B_1 (upstream) will be computed and the hypotheses proposed for the whole molecular and cellular mechanisms of cognition in the future.

Declarations
Ethics approval and consent to participate Not applicable.