nirantk/geneticsQA-train huggingface dataset:
Question: What is known about the Kub5-Hera/RPRD1B interactome?

Context:
The Kub5-Hera/RPRD1B interactome: a novel role in preserving genetic stability by regulating DNA mismatch repair
Ku70-binding protein 5 (Kub5)-Hera (K-H)/RPRD1B maintains genetic integrity by concomitantly minimizing persistent R-loops and promoting repair of DNA double strand breaks (DSBs)
The Kub5-Hera/RPRD1B interactome: a novel role in preserving genetic stability by regulating DNA mismatch repair.

Answer: Ku70-binding protein 5 (Kub5)-Hera (K-H)/RPRD1B maintains genetic integrity by concomitantly minimizing persistent R-loops and promoting repair of DNA double strand breaks (DSBs). Thus, the Kub5-Hera/RPRD1B interactome plays a novel role in preserving genetic stability by regulating DNA mismatch repair.
Question: What is the definition of autophagy?

Context:
autophagy, a process in which de novo formed membrane enclosed vesicles engulf and consume cellular components
As a general definition, autophagy encompasses a range of processes in which the cell degrades parts of itself within the lysosome (or the analogous organelle, the vacuole, in yeast and plants), followed by the release and reuse of the breakdown products
definition of autophagy is the following: all processes in which intracellular material is degraded within the lysosome/vacuole and where the macromolecular constituents are recycled
Autophagic PCD in animals is defined as being accompanied by an increase in the number of autophagosomes, autolysosomes, and small lytic vacuoles produced by autolysosomes
utophagy is the endogenous, tightly regulated cellular "housekeeping" process responsible for the degradation of damaged and dysfunctional cellular organelles and protein aggregates
utophagy has been predominantly studied as a nonselective self-digestion process that recycles macromolecules and produces energy in response to starvation
utophagy is a ubiquitous eukaryotic cytoplasmic quality and quantity control pathway
utophagy is a catabolic trafficking pathway for bulk destruction and turnover of long-lived proteins and organelles via regulated lysosomal degradation.
 non-apoptotic programmed cell death, such as autophagy 
utophagy and senescence share a number of characteristics, which suggests that both responses could serve to collaterally protect the cell from the toxicity of external stress such as radiation and chemotherapy and internal forms of stress such as telomere shortening and oncogene activation

Answer: There are several definitions of autophagy. Among them, autophagy can be defined as a non- apoptotic programmed cell death that consists on a catabolic trafficking pathway for bulk destruction and turnover of long-lived proteins and organelles via regulated lysosomal degradation.
Question: Which cells secretes alpha defensin 5?

Context:
The major tissue in which HD5 is expressed is the crypt of the small intestine, an anaerobic niche that should allow for substantial pools of both oxidized and (partly) reduced HD5. 
Human α-defensin 5 (HD5) exhibits broad spectrum antimicrobial activity and plays an important role in mucosal immunity of the small intestine.
Human enteric α-defensins (HD5 and HD6), major antimicrobial peptides produced by Paneth cells in the intestine, play important roles in intestinal innate immunity.
Human α-defensin 5 (HD5), the most abundant enteric antimicrobial peptide,
HD5, naturally present at very high concentrations in the mucosa of the small intestine, 
Human α-defensin 5 (HD5) is an innate immune effector peptide secreted by epithelial cells in the genitourinary tract
Human α-defensin 5 (HD5) is a 32-residue cysteine-rich host-defense peptide that exhibits broad-spectrum antimicrobial activity and contributes to innate immunity in the human gut and other organ systems. 
The concentrations of lactoferrin and defensins in preterm breast milk have antimicrobial activity against common neonatal pathogens.

Answer: Human enteric α-defensins (HD5 and HD6), major antimicrobial peptides produced by Paneth cells in the intestine, play important roles in intestinal innate immunity.
Exact answer: Intestinal Paneth cells secretes alpha-defensin 5
Question: Which thyroid hormone transporter is implicated in thyroid hormone resistance syndrome?

Context:
Hemizygous MCT8 mutations in males cause severe psychomotor retardation, known as the Allan-Herndon-Dudley syndrome (AHDS), and abnormal serum TH levels. AHDS thus represents a type of TH resistance caused by a defect in cellular TH transport.
Novel mutation in MCT8 gene in a Brazilian boy with thyroid hormone resistance and severe neurologic abnormalities.
When thyroid hormone production was reduced by PTU, high doses of LT(4) (3.7 microg/kg.d) were needed to normalize serum TSH, confirming that mutation of MCT8 is a cause of resistance to thyroid hormone
One, producing severe psychomotor defects in > 100 males from 26 families, is caused by mutations in the cell-membrane transporter of TH, MCT8

Answer: thyroid hormone transporter MCT8 is implicated in thyroid hormone resistance syndrome
Hemizygous MCT8 mutations cuases TH resistance syndrome in males characterized by severe psychomotor retardation, known as the Allan-Herndon-Dudley syndrome (AHDS).
Exact answer: monocarboxylate transporter 8
TH monocarboxylate transporter 8 (MCT8) mutation is implicated in the TH resistance syndrome
MCT8
Question: Describe Exploding head syndrome.

Context:
Exploding head syndrome is characterized by the perception of loud noises during sleep-wake or wake-sleep transitions.
Exploding head syndrome is characterized by the perception of abrupt, loud noises when going to sleep or waking up.
BACKGROUND: Exploding head syndrome (EHS) is characterized by attacks of a sudden noise or explosive feeling experienced in the head occurring during the transition from wake to sleep or from sleep to wake.
INTRODUCTION: Exploding head syndrome (EHS) is a rare parasomnia in which affected individuals awaken from sleep with the sensation of a loud bang.
Exploding head syndrome (EHS) is characterized by attacks of a sudden noise or explosive feeling experienced in the head occurring during the transition from wake to sleep or from sleep to wake.
Exploding head syndrome (EHS) attacks are characterized by the sensation of sudden loud banging noises, and are occasionally accompanied by the sensation of a flash light.
Exploding head syndrome (EHS) is characterized by attacks of a sudden noise or explosive feeling experienced in the head occurring during the transition from wake to sleep or from sleep to wake.We present six new cases extending the clinical experience with the syndrome
Exploding head syndrome (EHS) is a rare parasomnia in which affected individuals awaken from sleep with the sensation of a loud bang
Exploding head syndrome (EHS) attacks are characterized by the sensation of sudden loud banging noises, and are occasionally accompanied by the sensation of a flash light. 
Exploding head syndrome (EHS) is characterized by attacks of a sudden noise or explosive feeling experienced in the head occurring during the transition from wake to sleep or from sleep to wake.We present six new cases extending the clinical experience with the syndrome.

Answer: Exploding head syndrome is characterized by the perception of abrupt, loud noises when going to sleep or waking up.
Question: What are the functions of sorting nexin 27?

Context:
Knockdown of SNX27 by siRNA in HEK293 cells raised MRP4 expression on the plasma membrane, increased the extrusion of 6-[(14)C]mercaptopurine, an MRP4 substrate, and conferred resistance against 6-[(14)C]mercaptopurine.
Sorting nexin 27 (SNX27) is a 62-kDa protein localized to early endosomes and known to regulate the intracellular trafficking of ion channels and receptors.
Finally, migration assays revealed that depletion of SNX27 from HeLa and mouse principal kidney cortical collecting duct cells significantly decreases cell motility. We propose a model by which SNX27 regulates trafficking of β-Pix to focal adhesions and thereby influences cell motility.
We found that SNX27a redirected part of 5-HT4(a)R to early endosomes.
sorting nexin 27 (SNX27), a recently described member of a protein family involved in intracellular trafficking,
SNX27 co-localized with transferrin receptor-positive vesicles, pointing to its participation in T cell endocytic recycling.
This protein is a unique member of the sorting nexin family of proteins, a group generally involved in the endocytic and intracellular sorting machinery
These previously unreported results indicate that SNX27 is a participant in NK cell polarization, as a mediator or target of the mechanism.
Like most sorting nexins, SNX27 possesses a functional PX domain that selectively binds the membrane phospholipid phosphatidylinositol-3-phosphate (PI3P) and is important for trafficking to the early endosome.
This is consistent with a role of SNX27 as a general regulator for sorting of membrane proteins containing a PDZ-binding motif, and its absence may alter the trafficking of these proteins, leading to growth and survival defects.
Sorting nexin 27 (SNX27) belongs to the sorting nexin family of proteins, which participate in vesicular and protein trafficking. Similarly to all sorting nexin proteins, SNX27 has a functional PX domain that is important for endosome binding, but it is the only sorting nexin with a PDZ domain.
These results identify SNX27 as a PDZ-containing component of the T cell immunological synapse, and demonstrate a role for this protein in the regulation of the Ras-ERK pathway, suggesting a functional relationship between SNX27 and DGKζ.
Sorting nexins have been implicated in trafficking of proteins through endosomal compartments.

Answer: Sorting nexin 27 (SNX27) regulates endocytic sorting/recycling and intracellular trafficking of ion channels and receptors.
Question: What is the effect of SAHA treatment in Huntington's disease?

Context:
Suberoylanilide hydroxamic acid, a histone deacetylase inhibitor, ameliorates motor deficits in a mouse model of Huntington's disease
To further explore the therapeutic potential of HDAC inhibitors, we have conducted preclinical trials with suberoylanilide hydroxamic acid (SAHA), a potent HDAC inhibitor, in the R6/2 HD mouse model. We show that SAHA crosses the blood-brain barrier and increases histone acetylation in the brain
SAHA dramatically improved the motor impairment in R6/2 mice, clearly validating the pursuit of this class of compounds as HD therapeutics.
Suberoylanilide hydroxamic acid, a histone deacetylase inhibitor, protects dopaminergic neurons from neurotoxin-induced damage
Suberoylanilide hydroxamic acid (SAHA) was the first HDAC inhibitor approved by the Food and Drug Administration for the sole use of cancer therapy. The purpose of this study was to explore the potential new indications of SAHA for therapy of neurodegenerative diseases in in vitro Parkinson's disease models
The novel neurotrophic and neuroprotective effects of SAHA demonstrated in this study suggest that further study of this HDAC inhibitor could provide a new therapeutic approach to the treatment of neurodegenerative diseases
SAHA displayed dose- and time-dependent prolongation of the survival and protection against neurotoxin-induced neuronal death of dopaminergic neurons
neuroprotective effects of SAHA were mediated in part by promoting release of neurotrophic factors from astroglia through inhibition of histone deacetylation

Answer: Suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor, protects dopaminergic neurons from neurotoxin-induced damage. SAHA is predominantly an inhibitor of class I HDACs. However, it can also bind to class IIa HDACs and has been shown to degrade class IIa HDACs at the protein level in vitro. The neuroprotective effects of SAHA were mediated in part by promoting release of neurotrophic factors from astroglia through inhibition of histone deacetylation. SAHA can lead to the degradation of class IIa HDACs 4 and 5 via RANBP2 mediated proteasome degradation in vitro.
Question: Which is the mechanism used by bacteria to induce tumors in Arabidopsis?

Context:
Agrobacterium tumefaciens causes crown gall disease in a wide range of plant species. The neoplastic growth at the infection sites is caused by transferring, integrating, and expressing transfer DNA (T-DNA) from A. tumefaciens into plant cells
 gall tumors develop after integration of the T-DNA of virulent Agrobacterium tumefaciens strains into the plant genome
robacterium tumefaciens is a plant pathogenic bacterium that causes neoplastic growths, called 'crown gall', via the transfer and integration of transferred DNA (T-DNA) from the bacterium into the plant genome.
grobacterium tumefaciens causes crown gall disease by transferring and integrating bacterial DNA (T-DNA) into the plant genome
ransformation of plant cells with T-DNA of virulent agrobacteria is one of the most extreme triggers of developmental changes in higher plants.
grobacterium tumefaciens infects plants and induces the formation of tumors called "crown galls" by integrating the transferred-DNA (T-DNA) region of the Ti-plasmid into the plant nuclear genome
-DNA nuclear import is a central event in genetic transformation of plant cells by Agrobacterium
grobacterium tumefaciens Chry5, which is particularly virulent on soybeans, induces tumors 
 have identified T-DNA tagged Arabidopsis mutants that are resistant to transformation by Agrobacterium tumefaciens (rat mutants
grobacterium tumefaciens induces crown gall tumors on plants by transferring a nucleoprotein complex, the T-complex, from the bacterium to the plant cell
The recalcitrance of another ecotype occurs at a late step in T-DNA transfer

Answer: The bacteria Agrobacterium tumefaciens infects Arabidopsis, as well as other plants, and induces the formation of tumors by integrating the transferred-DNA (T-DNA) region of the Ti-plasmid into the plant nuclear genome.
Question: What is the RESID database?

Context:
The RESID Database of Protein Modifications as a resource and annotation tool.
The RESID Database of Protein Modifications is a comprehensive collection of annotations and structures for protein modifications and cross-links including pre-, co-, and post-translational modifications
The RESID Database is a comprehensive collection of annotations and structures for protein pre-, co- and post-translational modifications including amino-terminal, carboxyl-terminal and peptide chain cross-link modifications.
The RESID Database is a comprehensive collection of annotations and structures for protein post-translational modifications including N-terminal, C-terminal and peptide chain cross-link modifications. 
The RESID Database contains supplemental information on post-translational modifications for the standardized annotations appearing in the PIR-International Protein Sequence Database. 
The RESID Database of protein structure modifications.

Answer: The RESID Database of Protein Modifications is a comprehensive collection of annotations and structures for protein modifications and cross-links including pre-, co-, and post-translational modifications
Exact answer: The RESID Database of Protein Modifications is a comprehensive collection of annotations and structures for protein modifications and cross-links including pre-, co-, and post-translational modifications
Question: Is there evidence for de novo genesis of enhancers in vertebrates?

Context:
De novo genesis of enhancers in vertebrates.
Evolutionary innovation relies partially on changes in gene regulation. While a growing body of evidence demonstrates that such innovation is generated by functional changes or translocation of regulatory elements via mobile genetic elements, the de novo generation of enhancers from non-regulatory/non-mobile sequences has, to our knowledge, not previously been demonstrated. Here we show evidence for the de novo genesis of enhancers in vertebrates. For this, we took advantage of the massive gene loss following the last whole genome duplication in teleosts to systematically identify regions that have lost their coding capacity but retain sequence conservation with mammals. We found that these regions show enhancer activity while the orthologous coding regions have no regulatory activity. These results demonstrate that these enhancers have been de novo generated in fish. By revealing that minor changes in non-regulatory sequences are sufficient to generate new enhancers, our study highlights an important playground for creating new regulatory variability and evolutionary innovation.
Here we show evidence for the de novo genesis of enhancers in vertebrates.
While a growing body of evidence demonstrates that such innovation is generated by functional changes or translocation of regulatory elements via mobile genetic elements, the de novo generation of enhancers from non-regulatory/non-mobile sequences has, to our knowledge, not previously been demonstrated.
While a growing body of evidence demonstrates that such innovation is generated by functional changes or translocation of regulatory elements via mobile genetic elements, the de novo generation of enhancers from non-regulatory/non-mobile sequences has, to our knowledge, not previously been demonstrated
While a growing body of evidence demonstrates that such innovation is generated by functional changes or translocation of regulatory elements via mobile genetic elements, the de novo generation of enhancers from non-regulatory/non-mobile sequences has, to our knowledge, not previously been demonstrated. Here we show evidence for the de novo genesis of enhancers in vertebrates. For this, we took advantage of the massive gene loss following the last whole genome duplication in teleosts to systematically identify regions that have lost their coding capacity but retain sequence conservation with mammals. 
Here we show evidence for the de novo genesis of enhancers in vertebrates. 
While a growing body of evidence demonstrates that such innovation is generated by functional changes or translocation of regulatory elements via mobile genetic elements, the de novo generation of enhancers from non-regulatory/non-mobile sequences has, to our knowledge, not previously been demonstrated. Here we show evidence for the de novo genesis of enhancers in vertebrates.

Answer: Yes.
Exact answer: yes
Question: What genetic alterations are commonly associated with Diffuse Midline Gliomas, aside from IDH1 mutation and EGFR amplification, and often linked to p53 overexpression, ATRX loss, and monosomy 10?

Context:
 transgenes are sufficient to reduce the amounts of H3K27me3 in vitro and in vivo.", "In contrast, thalamic gliomas with wild-type H3F3A had DNA methylation profiles similar to those of hemispheric glioblastomas.CONCLUSION: We found that high-grade thalamic gliomas from young adults, like those from children and adolescents, frequently had H3F3A K27M.", "Gliomas with H3F3A K27M from pediatric or young adult patients had similar, characteristic DNA methylation profiles.", "Although the K27M mutation was frequently observed in adult brainstem and thalamic gliomas, this mutation tended to be associated with a poorer prognosis in brainstem gliomas but not in thalamic gliomas.", "Diffuse Midline Gliomas with Histone H3-K27M Mutation: A Series of 47 Cases Assessing the Spectrum of Morphologic Variation and Associated Genetic Alterations.", "In this series, histone H3-K27M mutation was mutually exclusive with IDH1 mutation and EGFR amplification, rarely co-occurred with BRAF-V600E mutation, and was commonly associated with p53 overexpression, ATRX loss (except in pontine gliomas), and monosomy 10.", "The H3.3 K27M mutation results in a poorer prognosis in brainstem gliomas than thalamic gliomas in adults.", "K27M mutation in histone H3.3 defines clinically and biologically distinct subgroups of pediatric diffuse intrinsic pontine gliomas.", "Recently, sequencing of tumor cells revealed that histone H3 is frequently mutated in pediatric HGG, with up to 78\u00a0% of diffuse intrinsic pontine gliomas (DIPGs) carrying K27M and 36\u00a0% of non-brainstem gliomas carrying either K27M or G34R/V mutations.", "Interestingly, the G34 mutations, the K36M mutations, and the majority of K27M mutations occur in genes encoding the replacement histone H3.3."]

Answer: The H3.3 K27M mutation is commonly associated with Diffuse Midline Gliomas, aside from IDH1 mutation and EGFR amplification, and often linked to p53 overexpression, ATRX loss, and monosomy 10.
Question: Is ABCE1 involved in ribosomal recycling?

Context:
Ribosome recycling orchestrated by the ATP binding cassette (ABC) protein ABCE1 can be considered as the final-or the first-step within the cyclic process of protein synthesis, connecting translation termination and mRNA surveillance with re-initiation.
 Recent studies have identified ABCE1 as a ribosome-recycling factor important for translation termination in mammalian cells, yeast and also archaea.
d a termination/prerecycling complex containing eRF1-ABCE1
ABCE1, a eukaryotic ribosome recycling factor

Answer: Yes, recent studies have identified ABCE1 as a ribosome-recycling factor important for translation termination in mammalian cells, yeast and also archaea
Exact answer: yes
Question: How does adrenergic signaling affect thyroid hormone receptors?

Context:
PE, in the absence of T3, resulted in 5.0 fold increase in TRalpha1 expression in nucleus and 2.0 fold decrease in TRalpha1 expression in cytosol, P<0.05.
nuclear TRalpha1 is overexpressed after prolonged activation of the alpha1- adrenergic signalling by PE. This response seems to be an ERK kinase dependent process.

Answer: alpha1- adrenergic signalling  increases  TRalpha1 expression in nucleus and  decreases  TRalpha1 expression in cytosol.
Question: What is the association between number of pregnancies and rheumatoid arthritis

Context:
In this unique population, greater parity significantly reduced the odds of RA;
an early age at first birth increased the odds, and the postpartum period was confirmed as high risk for RA onset. The protective effect of repeated exposure to the ameliorating hormonal and immunological changes of pregnancy may counterbalance the effect of early exposure to the postpartum reversal of these changes.
We found an inverse correlation between the number of pregnancies and age at onset of RA
A larger number of pregnancies and late menopause show a protective effect, delaying the onset of the disease.
Since the landmark study on rheumatoid arthritis, many reports have suggested that physiological changes during pregnancy often induce remission of systemic and cutaneous inflammatory diseases.
Literature review shows that at best, there are weak negative associations between current estrogen use and RA, and no association with nulliparity and infertility.
It appears that infertility, the number of pregnancies, and pregnancy outcome are not strongly associated with the risk of developing RA in women of childbearing age. However, in this study there may have been selection biases in the women with RA and the controls that differentially could have affected their reproductive outcomes. Thus, a true association could have been missed. Most other published studies find no association between nulliparity and RA.
Number of pregnancies and children, however, were significantly higher in controls

Answer: Greater parity significantly reduced the odds of RA. A larger number of pregnancies and late menopause show a protective effect, delaying the onset of the disease.
Question: Can valproic acid act as an activator of AMPK?

Context:
Here we demonstrate that VPA is a novel activator of AMP-activated protein kinase (AMPK), a key regulator of cellular metabolism, using primary mouse and human hepatocytes.
These studies are the first to establish VPA and its metabolites as in vitro activators of AMPK.

Answer: Yes, valproic acid canact as an activator of AMPK.
VPA is a novel activator of AMP-activated protein kinase (AMPK)
Exact answer: yes