nirantk/geneticsQA-train huggingface dataset:
Question: How do synapsins affect neuronal development?

Context:
Synapsin is an evolutionarily conserved presynaptic phosphoprotein.
Synapsins as a family of presynaptic terminal phosphoprotein participates in neuronal development
Synapsin III (SynIII) is a phosphoprotein
The neuronal phosphoprotein synapsin III
Synapsin II is a member of the neuronal phosphoprotein family.
phosphoprotein synapsin
Synapsin is an evolutionarily conserved presynaptic phosphoprotein.
Synapsins as a family of presynaptic terminal phosphoprotein participates in neuronal development
Synapsin III (SynIII) is a phosphoprotein
The neuronal phosphoprotein synapsin III
Synapsin II is a member of the neuronal phosphoprotein family.
phosphoprotein synapsin

Answer: Synapsins, as a family of presynaptic terminal phosphoproteins, participate in neuronal development by playing a role in synaptic function and neurotransmitter release. Specifically, Synapsin III (SynIII) and Synapsin II, both phosphoproteins, are involved in regulating synaptic vesicle trafficking and neurotransmitter release, contributing to the development and function of neuronal networks.
Question: What is a disordered protein?

Context:
Intrinsically disordered proteins (IDPs) are ubiquitously involved in cellular processes and often implicated in human pathological conditions. The critical biological roles of these proteins, despite not adopting a well-defined fold, encouraged structural biologists to revisit their views on the protein structure-function paradigm.
Intrinsically disordered proteins (IDPs) frequently function in protein interaction networks that regulate crucial cellular signaling pathways. Many IDPs undergo transitions from disordered conformational ensembles to folded structures upon binding to their cellular targets.
The intrinsically disordered protein (IDP) stathmin plays an important regulatory role in cytoskeletal maintenance through its helical binding to tubulin and microtubules. However, it lacks a stable fold in the absence of its binding partner. 
Intrinsically disordered proteins lack stable tertiary and/or secondary structures under physiological conditions in vitro. Intrinsically disordered proteins undergo significant conformational transitions to well folded forms only on binding to partner.
DisCons is an openly accessible sequence analysis tool that identifies and highlights structurally disordered segments of proteins where the conformational flexibility is conserved across homologs, and therefore potentially functional. 

Answer: Intrinsically disordered proteins lack stable tertiary and/or secondary structures under physiological conditions in vitro. Intrinsically disordered proteins undergo significant conformational transitions to well folded forms only on binding to partner.
Question: What is the methyl donor of DNA (cytosine-5)-methyltransferases?

Context:
The product of the dcm gene is the only DNA cytosine-C5 methyltransferase of Escherichia coli K-12; it catalyses transfer of a methyl group from S-adenosyl methionine (SAM) to the C-5 position of the inner cytosine residue of the cognate sequence CCA/TGG. 
Deoxycytosine methylase (Dcm) enzyme activity causes mutagenesis in vitro either directly by enzyme-induced deamination of cytosine to uracil in the absence of the methyl donor, S-adenosylmethionine (SAM), or indirectly through spontaneous deamination of [5-methyl]cytosine to thymine
In the absence of DNA substrate, the DNA methyltransferase (MTase) M.BspRI can methylate itself using the methyl donor S-adenosyl-L-methionine (AdoMet). The methyl group is transferred to two Cys residues of the MTase.
The reaction is fairly insensitive to the methyl donor in the reaction, S-adenosylmethionine.
Formation of the complex was dependent upon the presence of the methyl donor S-adenosylmethionine, suggesting that it comprises an enzyme-linked 5-substituted dihydrocytosine moiety in DNA. 
The DNA (cytosine-5)-methyltransferase (m5C-MTase) M.BspRI is able to accept the methyl group from the methyl donor S-adenosyl-L-methionine (AdoMet) in the absence of DNA. Transfer of the methyl group to the enzyme is a slow reaction relative to DNA methylation. S
Here, we report the structure of HhaI methyltransferase in complex with DNA containing a south-constrained abasic carbocyclic sugar at the target site in the presence of the methyl donor byproduct AdoHcy.

Answer: S-adenosyl-L-methionine (AdoMet, SAM) is the methyl donor of DNA (cytosine-5)-methyltransferases. DNA (cytosine-5)-methyltransferases catalyze the transfer of a methyl group from S-adenosyl-L-methionine to the C-5 position of cytosine residues in DNA.
Exact answer: S-adenosyl-L-methionine
Question: Which neuroendocrine tumors are associated with specific tumor syndromes?

Context:
Pheochromocytomas are neuroendocrine tumors of the adrenal medulla which can occur either sporadically or in the context of hereditary tumor syndromes
Pheochromocytomas (PCCs) and paragangliomas (PGLs) are rare neuroendocrine tumors of the adrenal glands and the sympathetic and parasympathetic paraganglia. They can occur sporadically or as a part of different hereditary tumor syndromes
Pancreatic neuroendocrine tumors (PNETs) are a characteristic feature of the tumor syndromes multiple endocrine neoplasia type 1 (MEN-1) and von Hippel-Lindau disease (VHL)
This review focuses on hereditary syndromes with neuroendocrine tumors, including multiple endocrine neoplasia types 1 and 2, Von Hippel-Lindau disease, neurofibromatosis type 1, Carney complex, pheochromocytoma-paraganglioma syndrome, and familial nonmedullary thyroid carcinoma. In addition, several individual neuroendocrine tumors are described, such as medullary thyroid carcinoma, gastroenteropancreatic tumors, pheochromocytoma, and paraganglioma, emphasizing specific histopathologic characteristics
Neuroendocrine tumors (NETs) are a heterogeneous group of benign and malignant neoplasias, detectable in the context of hereditary tumor syndromes in up to 30% of cases
RET gene analysis can identify individuals with a very high risk to develop familial medullary cancer (MEN2)
In addition, several individual neuroendocrine tumors are described, such as medullary thyroid carcinoma, gastroenteropancreatic tumors, pheochromocytoma, and paraganglioma, emphasizing specific histopathologic characteristics

Answer: Neuroendocrine tumors are a heterogeneous group of benign and malignant neoplasias, detectable in the context of hereditary tumor syndromes in up to 30% of cases. Neuroendocrine tumors include medullary thyroid carcinoma, gastroenteropancreatic tumors, pheochromocytoma, and paraganglioma.
Exact answer: medullary thyroid carcinoma, gastroenteropancreatic tumors, pheochromocytoma, paraganglioma
Question: Does resveratrol reduce cardiac remodeling?

Context:
In conclusion, resveratrol attenuated cardiac oxidative damage and left ventricular remodeling and enhanced the decreased expression of SIRT1 in hearts of old rats with emphysema and thus might be a therapeutic modality for cardiac injury complicated in chronic obstructive pulmonary disease (COPD).
In conclusion, resveratrol is a beneficial pharmacological tool that augments autophagy to bring about reverse remodeling in the postinfarction heart.
Resveratrol administration reduced atrial CSPC loss, succeeded in preserving the functional abilities of CSPCs and mature cardiac cells, improved cardiac environment by reducing inflammatory state and decreased unfavorable ventricular remodeling of the diabetic heart, leading to a marked recovery of ventricular function. These findings indicate that RSV can constitute an adjuvant therapeutic option in DCM prevention.

Answer: Resveratrol attenuates left ventricular remodeling.
Resveratrol is a beneficial pharmacological tool that augments autophagy to bring about reverse remodeling in the postinfarction heart.
Resveratrol administration improved cardiac environment by reducing inflammatory state and decreased unfavorable ventricular remodeling of the diabetic heart, leading to a marked recovery of ventricular function.
Resveratrol can constitute an adjuvant therapeutic option in prevention of dilated cardiomyopathy.
Most of the evidence shows that Resveratrol supresses cardiac remodeling.
Exact answer: yes
Question: List the results of mutated casein kinase 1 epsilon. 

Context:
These results demonstrate a role for Csnk1e in regulating not only the timing of sleep, but also the REM sleep amount and NREM sleep architecture, and support Csnk1e as a causal gene in the sleep QTL on chromosome 15.
mutations of CK1epsilon found in breast cancer can suppress Wnt/beta-catenin as well as promote the Wnt/Rac-1/JNK and Wnt/NFAT pathways, thus contributing to breast cancer development via effects on cell adhesion and migration
results in a short circadian period, abnormal entrainment to light cycles, and potentiated resetting responses to light.
We now demonstrate that the mutation results in a heightened sensitivity to light, suggesting that CK1epsilon also regulates the photic entrainment pathway.

Answer: Mutation in casein kinase 1 epsilon results in a short circadian period, abnormal entrainment to light cycles, and potentiated resetting responses to light.
Mutations of CK1epsilon found in breast cancer can suppress Wnt/beta-catenin as well as promote the Wnt/Rac-1/JNK and Wnt/NFAT pathways, thus contributing to breast cancer development via effects on cell adhesion and migration.
Csnk1e is regulating not only the timing of sleep, but also the REM sleep amount and NREM sleep architecture.
Exact answer: short circadian period, abnormal entrainment to light cycles, potentiated resetting responses to light, REM sleep amount, NREM sleep architecture, effects on cell adhesion, effects on cell migration, timing of sleep
Question: Where are Paneth cells located?

Context:
The intestinal stem cell niche comprises both epithelial cells, in particular the Paneth cell, 
Paneth cells have been reported in colorectal adenomas and adenocarcinomas;
 injury to Paneth cells (PCs) in the intestinal crypts
resence of Paneth cells at the bottom of the crypts of Lieberkühn.
Paneth cells at the crypt base 
 Paneth cells (crypt base columnar cells (CBCCs))

Answer: Paneth cells are located in the intestinal crypt base columnar cells (CBCCs).
Exact answer: in the intestinal crypt base columnar cells
Question: How many topological associated domains are contained in the human Hox cluster?

Context:
Initially, Hox clusters are organized as single chromatin compartments containing all genes and bivalent chromatin marks.
Transcriptional activation is associated with a dynamic bi-modal 3D organization, whereby the genes switch autonomously from an inactive to an active compartment.

Answer: transcriptional activation is associated with a dynamic bi-modal 3d organization, whereby the genes switch autonomously from an inactive to an active compartment.
Initially, Hox clusters are organized as single chromatin compartments containing all genes and bivalent chromatin marks. Transcriptional activation is associated with a dynamic bi-modal 3D organization, whereby the genes switch autonomously from an inactive to an active compartment. 
, hox clusters are organized as single chromatin compartments containing all genes and bivalent chromatin marks. . activation is associated with a dynamic bi-modal 3d organization , whereby the genes switch autonomously from an inactive to an active compartment. . 
Initially, Hox clusters are organized as single chromatin compartments containing all genes and bivalent chromatin marks. Transcriptional activation is associated with a dynamic bi-modal 3D organization, whereby the genes switch autonomously from an inactive to an active compartment.
Exact answer: two, 2
Question: Which is the molecular mechanism underlying K-ras alterations in carcinomas?

Context:
activating mutations in KRAS are identified in most pancreatic cancers
Mutations at codon 12 of the K-ras gene are present in 65%-100% of carcinomas of human exocrine pancreas and could be used as a potential tumor marker at the tissue level.
Activating point mutations in the K-Ras oncogene are among the most common genetic alterations in pancreatic cancer, occurring early in the progression of the disease.
Activating K-ras mutations are found in approximately 90% of pancreatic carcinomas and may contribute to the poor prognosis of these tumors.
Five of the seven duct lesions harbored activating point mutations in codon 12 of K-ras; a G to A transition was found in four and a G to C transversion in one.
Ki-RAS mutations in 38% of the overall series
KRAS exon 2 mutations were detected in a total of 62 patients with the two methods combined, comprising 11 different mutant alleles.
gain-of-function mutations in ras genes were the first specific genetic alterations identified in human cancer

Answer: Activating point mutations most frequently in codon 12
Exact answer: Point mutations
Question: Which disorders are associated to mutated Hepcidin (HAMP)?

Context:
juvenile hemochromatosis due to hemojuvelin and hepcidin mutation
 Mutations in all of the currently known genes implicated in non-HFE HH (hemojuvelin, hepcidin, transferrin receptor 2, and ferroportin) have been reported in patients from the Asia-Pacific region.
 In conclusion, HAMP and hemojuvelin mutations are rare among Spanish HH patients, and their impact in this population is not significant.
Juvenile hemochromatosis (JH) is the most severe form, usually caused by mutations in hemojuvelin (HJV) or hepcidin (HAMP). 
We have identified novel mutations in HJV, HAMP, and SLC40A1 in countries not normally associated with hereditary hemochromatosis (Pakistan, Bangladesh, Sri Lanka, and Thailand).
In humans, loss of TfR2, HJV, and hepcidin itself or FPN mutations result in full-blown hemochromatosis. 
Targeting hepcidin with replacement therapy to decrease iron may be a treatment of not only HCV, HH, and alcoholic cirrhosis, but also PCT.
Hepcidin deficiency underlies iron overload in HFE-hemochromatosis as well as in several other genetic iron excess disorders, such as hemojuvelin or hepcidin-related hemochromatosis and transferrin receptor 2-related hemochromatosis. 
In addition to HFE gene, mutations in the genes that encode hemojuvelin (HJV), hepcidin (HAMP), transferrin receptor 2 (TFR2) and ferroportin (SLC40A1) have been associated with regulation of iron homeostasis and development of HH

Answer: Juvenile hemochromatosis (JH) is the most severe form of heriditary hemochromatosis, usually caused by mutations in hemojuvelin (HJV) or hepcidin (HAMP).
Exact answer: juvenile hemochromatosis
Question: Which gene is involved in CADASIL?

Context:
leukoencephalopathy (CADASIL), the most common form of familial vascular dementia, is caused by mutations of the NOTCH3 gene
Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL) is a hereditary disease caused by mutations of the Notch3 gene encoding the Notch3 protein. Notch3 is involved in the regulation of apoptosis, modulating Fas-Ligand (Fas-L)- induced apoptosis.
: Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a small vessel disease of the brain caused by mutations in the NOTCH3 gene
Mutations in Notch3 gene are linked to cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), a disorder characterized by stroke and dementia in young adults
(CADASIL) is caused by mutations in the NOTCH3 gene and is clinically characterized by recurrent stroke, cognitive decline, psychiatric disturbances and migraine
To evaluate the role of apoptosis in the pathogenesis of brain lesions in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), a hereditary microangiopathy leading to cognitive decline and dementia, caused by mutations in the NOTCH3 gene.
NOTCH3 (Notch homolog 3), the gene involved in CADASIL, encodes a transmembrane receptor primarily expressed in systemic arterial smooth-muscle cells
(CADASIL) is a vascular dementing disease caused by mutations in the NOTCH3 gene, most which are missense mutations leading to an uneven number of cysteine residues in epidermal growth factor-like repeats in the extracellular domain of Notch3 receptor (N3ECD). 

Answer: Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), the most common form of familial vascular dementia, is caused by mutations of the NOTCH3 gene.
Exact answer: Notch3 gene
Question: Which package is available for analysing genomic interactions in R/Bioconductor?

Context:
r3Cseq: an R/Bioconductor package for the discovery of long-range genomic interactions from chromosome conformation capture and next-generation sequencing data.
We present r3Cseq, an R/Bioconductor package designed to perform 3C-seq data analysis in a number of different experimental designs. The package reads a common aligned read input format, provides data normalization, allows the visualization of candidate interaction regions and detects statistically significant chromatin interactions, thus greatly facilitating hypothesis generation and the interpretation of experimental results. We further demonstrate its use on a series of real-world applications
r3Cseq: an R/Bioconductor package for the discovery of long-range genomic interactions from chromosome conformation capture and next-generation sequencing data

Answer: r3Cseq is an R/Bioconductor package designed to perform 3C-seq data analysis in a number of different experimental designs. The package reads a common aligned read input format, provides data normalization, allows the visualization of candidate interaction regions and detects statistically significant chromatin interactions, thus greatly facilitating hypothesis generation and the interpretation of experimental results.
Exact answer: r3Cseq
Question: Which type of genes are modulated by SATB1?

Context:
Repression of the genome organizer SATB1 in regulatory T cells is required for suppressive function and inhibition of effector differentiation
SATB1, a genome organizer that regulates chromatin structure and gene expression, was crucial for the phenotype and function of T(reg) cells
Foxp3, acting as a transcriptional repressor, directly suppressed the SATB1 locus and indirectly suppressed it through the induction of microRNAs that bound the SATB1 3' untranslated region.
Release of SATB1 from the control of Foxp3 in T(reg) cells caused loss of suppressive function, establishment of transcriptional T(eff) cell programs and induction of T(eff) cell cytokines.
Consistent with previous reports in a non-superantigen in vivo anergy model, mRNA for CD18 and the transcription factor Satb1 (special AT-rich-binding protein 1) was increased in SEB-energized T cells. 

Answer: Lack of effector T cell (T(eff) cell) function and gain of suppressive activity by T(reg) cells are dependent on the transcriptional program induced by Foxp3. Here we report that repression of SATB1, a genome organizer that regulates chromatin structure and gene expression, was crucial for the phenotype and function of T(reg) cells. Release of SATB1 from the control of Foxp3 in T(reg) cells caused loss of suppressive function, establishment of transcriptional T(eff) cell programs and induction of T(eff) cell cytokines. At an Associative t-test threshold of P
Repression of the genome organizer SATB1 in regulatory T cells is required for suppressive function and inhibition of effector differentiation
Release of SATB1 from the control of Foxp3 in T(reg) cells caused loss of suppressive function, establishment of transcriptional T(eff) cell programs and induction of T(eff) cell cytokines.
Exact answer: it supresses cell cytokines and differentiation genes
Question: Is miR-126 involved in heart failure?

Context:
he miRNAs miR-126 and miR-508-5p are associated with the outcome of ICM and NICM patients with CHF. These two miRNAs could be useful in the diagnosis of CHF patients, and might provide novel targets for prevention and treatment of CHF.
The plasma concentration of miR-126 was negatively correlated with age and NYHA class, and could be a useful biomarker for heart failure.
In 10 patients with heart failure, plasma concentrations of miR-126 were up-regulated with improvement of the NYHA class from IV to III.

Answer: Yes, miR-126 is associated with heart failure.
Exact answer: yes
Question: What are the generic versions of Viagra

Context:
Sildenafil citrate (SIL)
generic sildenafil (Unison Laboratories, Thailand) was proved to have the same bioequivalent as in the original formula. The authors conducted a 12-week case series to study the efficacy and safety of Elonza (generic sildenafil)
Viagra tablets or generic versions containing sildenafil citrate

Answer: Sildenafil Citrate and Elonza in Thailand are the generic versions of Viagra
Question: What are the results of loss of the protein Lon1 in the plant Arabidopsis?

Context:
Knockout in Arabidopsis (Arabidopsis thaliana) leads to a significant growth rate deficit in both roots and shoots and lowered activity of specific mitochondrial enzymes associated with respiratory metabolism. 
loss of Lon1 significantly modifies respiratory function and plant performance by small but broad alterations in the mitochondrial proteome gained by subtly changing steady-state protein assembly, stability, and damage of a range of components that debilitate an anaplerotic role for mitochondria in cellular carbon metabolism.
the lack of Lon selective proteolysis leading to growth retardation and impaired seedling establishment can be attributed to defects in the oil reserve mobilization pathway. 
Loss of Lon1 in Arabidopsis changes the mitochondrial proteome leading to altered metabolite profiles and growth retardation without an accumulation of oxidative damage.
 a genetic screen was performed that led to the identification of Arabidopsis thaliana Lon1 protease mutants that exhibit a post-embryonic growth retardation phenotype.
mitochondria isolated from lon1 mutants had a lower capacity for respiration of succinate and cytochrome c via complexes II and IV, respectively. Furthermore, the activity of key enzymes of the tricarboxylic acid (TCA) cycle was significantly reduced. Additionally, mitochondria in lon1 mutants had an aberrant morphology. 
 AtLon1 protease in organelle biogenesis and seedling establishment.

Answer: Loss of Lon1 in Arabidopsis changes the mitochondrial proteome leading to altered metabolite profiles and growth retardation. Additionaly, seedling establishment is also impaired.
Exact answer: growth rate deficit in both roots and shoots
lowered activity of specific mitochondrial enzymes associated with respiratory metabolism
impaired seedling establishment
Question: What is a miR?

Context:
As novel molecules, microRNAs (miRs) take part in regulating protein-coding gene expression at the post-transcriptional level,
The discovery of microRNA (miRNA) regulation in tumorigenesis 
MiRs are small (~23 nt) noncoding RNAs that regulate gene expression by specifically interacting with the 3' untranslated region (UTR) of target gene mRNA to repress translation or enhance mRNA cleavage. 
The discovery of microRNAs (miRNAs) has opened an entire new avenue for drug development. These short (15-22 nucleotides) noncoding RNAs, which function in RNA silencing and posttranscriptional regulation of gene expression, have been shown to critically affect numerous pathways in both development and disease progression. 

Answer: The discovery of microRNAs (miRNAs) has opened an entire new avenue for drug development. These short (15-22 nucleotides) noncoding RNAs, which function in RNA silencing and posttranscriptional regulation of gene expression, have been shown to critically affect numerous pathways in both development and disease progression.
Exact answer: MiRs are small (~23 nt) noncoding RNAs