Persius/hicric huggingface dataset:
Suramin

# Overview
Suramin is an antimicrobial drug developed by Oskar Dressel and Richard Kothe of Bayer, Germany in 1916, and is still sold by Bayer under the brand name Germanin. The formula of suramin was kept secret by Bayer for commercial reasons, however, it was elucidated and published in 1924 by Ernest Fourneau and his team of the Pasteur Institute.
It is on the World Health Organization's List of Essential Medicines, a list of the most important medication needed in a basic health system.

# Medical uses

## Protozoa
It is used for treatment of human sleeping sickness caused by trypanosomes.

## Helminthiasis
It has been used in the treatment of onchocerciasis.

## Other
It has been investigated as treatment for prostate cancer.
Also, suramin as treatment for autism is being evaluated and there are promising results in adult mice.

# Adverse reactions
The most frequent adverse reactions are nausea and vomiting. 
About 90% of patients will get an urticarial rash that disappears in a few days without needing to stop treatment.  There is a greater than 50% chance of adrenal cortical damage, but only a smaller proportion will require lifelong corticosteroid replacement.  It is common for patients to get a tingling or crawling sensation of the skin with suramin.  Suramin will cause clouding of the urine which is harmless: patients should be warned of this to avoid them becoming alarmed.
Kidney damage and exfoliative dermatitis occur less commonly.
Suramin has been applied clinically to HIV/AIDS patients resulting in a significant number of fatal occurrences and as a result the application of this molecule was abandoned for this condition.

# Chemistry
The molecular formula of suramin is C51H40N6O23S6. It is a symmetric molecule in the center of which lies a urea (NHCONH) functional group. Suramin contains eight benzene rings, four of which are fused in pairs (naphthalene), four amide groups (in addition to the urea) and six sulfonic acid groups. When given as drug, it is usually as the sodium sulfonate, with six sodium ions on the sulfonate groups rather than hydrogens.

# Research
According to the National Cancer Institute there are no active clinical trials.
Suramin is also used in research as a broad-spectrum antagonist of P2 receptors and agonist of Ryanodine receptors.
Its effect on telomerase has been investigated.
It may have some activity against RNA viruses.
In addition to antagonism of P2 receptors, Suramin inhibits the activation of heterotrimeric G proteins in a variety of other GPCRs with varying potency.  It prevents the association of heteromeric G proteins and therefore the receptors guanine exchange functionality (GEF).  With this blockade the GDP will not release from the G subunit so it can not be replaced by a GTP and become activated. This has the effect of blocking downstream G protein mediated signaling of various GPCR proteins including rhodopsin, the A1 adenosine receptor, and the D2 dopamine receptor.
Sylvite
Sylvite is potassium chloride (KCl) in natural mineral form. It forms crystals in the isometric system very similar to normal rock salt, halite (NaCl). (The two are, in fact, isomorphous.  Sylvite is colorless to white with shades of yellow and red due to inclusions. It has a Mohs hardness of 2.5 and a specific gravity of 1.99. It has a refractive index of n=1.490) . Sylvite has a salty taste with a distinct bitterness.
Sylvite is one of the last evaporite minerals to precipitate out of solution. As such, it is only found in very dry saline areas. Its principal use is as a potassium fertilizer.
Sylvite is found in many evaporite deposits worldwide. Massive bedded deposits occur in New Mexico and western Texas, and in Utah in the US, but the largest world source is in Saskatchewan, Canada. The vast deposits in Saskatchewan, Canada were formed by the evaporation of a Devonian seaway. Sylvite is the official mineral of Saskatchewan.
Sylvite was first described in 1832 at Mt. Vesuvius near Napoli in Italy and named for the Dutch chemist, Francois Sylvius de le Boe (1614-1672).
Synemin
Synemin, also known as desmuslin, is a protein that in humans is encoded by the SYNM gene. Synemin is an intermediate filament (IF) family member. IF proteins are cytoskeletal proteins that confer resistance to mechanical stress and are encoded by a dispersed multigene family. This protein has been found to form a linkage between desmin, which is a subunit of the IF network, and the extracellular matrix, and provides an important structural support in muscle.

# Function
Synemin is an intermediate filament (IF) and, like other IFs, primarily functions to integrate mechanical stress and maintain structural integrity in eukaryotic cells. While it has been observed in a variety of cell types, it has been best studied in the sarcomere of skeletal myocytes. It localizes at the Z-disk and has been shown to bind to -dystrobrevin, -actinin, and desmin to act as a mechanical linker in transmitting force laterally throughout the tissue, especially between the contractile myofibrils and extracellular matrix. Synemin contributes to linkage between costameres and the contractile apparatus in skeletal muscle of synemin null animals.

# Properties
Synemin has properties very similar to the intermediate filament syncoilin. In particular, it binds to -dystrobrevin in the dystrophin-associated protein complex to act as a mechanical "linker" between the myofibrillar network and the cell membrane.

# Splice variants
Two splice variant isoforms of synemin exist,  and . Both isoforms have a very short N-terminal domain of 10 amino acids and a long C-terminal domain consisting of 1243 amino acids for the  isoform and 931 amino acids for the  isoform. An intronic sequence of the synemin  isoform is used as a coding sequence for synemin .

# History
The origin of the synemin/desmuslin naming convention is quite complex. In 1980, synemin was first identified in avian smooth muscle and was initially described as an IF-associated protein due to its colocalization and copurification with desmin and vimentin.  Subsequent to the cloning of chicken synemin, Mizuno and colleagues reported the cloning of a novel IF protein, human desmuslin, as an -dystrobrevin-interacting protein. Sequence analysis showed that human desmuslin was 32% identical and 11% similar to the amino acid sequence of chicken synemin, while the IF proteins vimentin and desmin are more than 80% identical across the same species. Although several parts were very similar between human desmuslin and chicken synemin, the low degree of conservation between these two proteins compared to other cloned IF proteins suggested that synemin was not the human desmuslin orthologue. In addition, unlike chicken synemin, in vitro coimmunoprecipitation assays could not detect an interaction between human desmuslin and -actinin.  In 2001, Titeux and colleagues reported the cloning of the  and  splice-varying isoforms of human synemin and showed that -synemin was identical to desmuslin. In 2014 was reported the first synemin -/- null animal.
Synulox
Synulox is a widely known brand name of Veterinary Antibiotic, used for treating infections mostly in the lungs, and nasal tract; and as a broad-spectrum antibiotic.  The drug is a compound of amoxicillin and Clavulanic Acid. See also Co-amoxiclav.
NB - All quantities shown below are combined - i.e. 500mg = 400mg Amoxicillin and 100mg Clavulanic Acid.

# Formulations
- 500mg Bolus: Large film-coated tablets. For the treatment of enteritis and navel ill in calves.
- Intramammary Suspension: Synulox + Prednisolone for intra-mammary infusion. For the treatment of mastitis in lactating cows.
- Palatable Drops: A powder for reconstitution for oral administration. A broad-spectrum antibiotic for dogs and cats.
- Palatable Tablets: Available as 50mg, 250mg and 500mg for oral administration. A broad-spectrum antibiotic for dogs and cats.
- Synulox Ready-To-Use Injection: Multi-purpose injectable formulation, recommended for respiratory tract infections, soft tissue infections, metritis and mastitis in cattle; respiratory tract infections, colibacillosis and mastitis, metritis & agalactia in pigs; respiratory tract infections, urinary tract infections, skin and soft tissue infections in dogs and cats.

# Bacterial Resistance
Bacterial antibiotic resistance is a growing problem in veterinary medicine. Clavulanic acid inactivates beta-lactamases which are a common resistance strategy in gram positive bacteria. 
Synulox is reported to be effective against clinical Klebsiella infections, but is not efficacious against Pseudomonas infections.
TACSTD2
Tumor-associated calcium signal transducer 2, also known as Trop-2 and as epithelial glycoprotein-1 antigen (EGP-1), is a protein that in humans is encoded by the TACSTD2 gene.
This intronless gene encodes a carcinoma-associated antigen defined by the monoclonal antibody GA733. This antigen is a member of a family including at least two type I membrane proteins. It transduces an intracellular calcium signal and acts as a cell surface receptor.
Mutations of this gene result in gelatinous drop-like corneal dystrophy, an autosomal recessive disorder characterized by severe corneal amyloidosis leading to blindness.
This antigen is the target of sacituzumab govitecan, an antibody-drug conjugate.
TAK 442

# TAK in Acute Coronary Syndrome Patients
On October 26, 2010 Takeda announced the top line data from a phase 2 study of TAK-442, an oral anticoagulant, biologically active factor Xa inhibitor (fXai). "This phase 2, multi-center, randomized double blind, placebo-controlled study conducted globally except in Japan was designed to evaluate the safety and tolerability of multiple doses and regimens (10mg BID to 120mg BID) of TAK-442 with placebo in subjects with a recent acute coronary syndrome (ACS) event, in addition to standard treatment (aspirin or dual anti-platelet therapy) for prevention of recurrent ischemic or thromboembolic events."
"The primary safety endpoint was defined as incidence of major bleeding events as defined by the thrombolysis in myocardial infarction (TIMI) scale, which were observed during the 24-week treatment period. In the lower doses there was a low rate of bleeding and in the higher dose groups, the bleeding rates were generally higher than that of placebo."
"The primary efficacy endpoint in the study was a composite of cardiovascular events, consisting of cardiovascular death, non-fatal myocardial infarction, non-fatal stroke or myocardial ischemia requiring hospitalization. The study did not demonstrate a positive trend to reduced risk of cardiovascular events for TAK-442 in this ACS patient population, and there was no evidence for a dose-response. Further analyses are underway to better understand the data as well as the possibility of other development strategies. Decisions are expected to be made as soon as the analysis is complete. "
TAS2R10
Taste receptor type 2 member 10 is a protein that in humans is encoded by the TAS2R10 gene.

# Function
This gene product belongs to the family of candidate taste receptors that are members of the G-protein-coupled receptor superfamily. These proteins are specifically expressed in the taste receptor cells of the tongue and palate epithelia. They are organized in the genome in clusters and are genetically linked to loci that influence bitter perception in mice and humans. In functional expression studies, they respond to bitter tastants. This gene maps to the taste receptor gene cluster on chromosome 12p13.
TAS2R10 is also expressed in the smooth muscle of human airways, along with several other bitter taste receptors. Their activation in these cells causes an increase in intracellular calcium ion, which in turn triggers the opening of potassium channels which hyperpolarize the membrane and cause the smooth muscle to relax. Hence, activation of these receptors leads to bronchodilation.
TAS2R14
Taste receptor type 2 member 14 is a protein that in humans is encoded by the TAS2R14 gene.

# Function
This gene product belongs to the family of candidate taste receptors that are members of the G-protein-coupled receptor superfamily. These proteins are specifically expressed in the taste receptor cells of the tongue and palate epithelia. They are organized in the genome in clusters and are genetically linked to loci that influence bitter perception in mice and humans. In functional expression studies, TAS2R14 responds to ()--thujone, the primary neurotoxic agent in absinthe, and picrotoxin, a poison found in fishberries. This gene maps to the taste receptor gene cluster on chromosome 12p13.
TAS2R14 is also expressed in the smooth muscle of human airways, along with several other bitter taste receptors. Their activation in these cells causes an increase in intracellular calcium ion, which in turn triggers the opening of potassium channels which hyperpolarize the membrane and cause the smooth muscle to relax. Hence, activation of these receptors leads to bronchodilation.
TAS2R16
TAS2R16 (taste receptor, type 2, member 16) is a human gene that encodes for a receptor that may play a role in the perception of bitterness.
The TAS2R16 gene is located on the long (q) arm of chromosome 7 at position 31.1 - 31.3, from base pair 122,228,764 to base pair 122,229,639.

# Clinical significance
Variants of this gene have been linked to an increased risk for alcohol dependence.
There is an East African origin for high salicin sensitivity, and thus sensitivity to bitterness in people from this region, with this phenotype matched to TAS2R16 variants.
TAS2R31
Taste receptor, type 2, member 31, also known as TAS2R31, is a protein which in humans is encoded by the TAS2R31 gene. This bitter taste receptor has been shown to respond to saccharin in vitro.
TAS2R31 is also expressed in the smooth muscle of human airways, along with several other bitter taste receptors. Their activation in these cells causes an increase in intracellular calcium ion, which in turn triggers the opening of potassium channels which hyperpolarize the membrane and cause the smooth muscle to relax. Hence, activation of these receptors leads to bronchodilation.
Polymorphisms in this gene have been associated with the perceived bitterness of sweetener acesulfame potassium.
TBC1D24
TBC1 domain family, member 24 is a protein that in humans is encoded by the TBC1D24 gene.

# Function
This gene encodes a protein with a conserved domain, referred to as the TBC domain, characteristic of proteins which interact with GTPases. TBC domain proteins may serve as GTPase-activating proteins for a particular group of GTPases, the Rab (Ras-related proteins in brain) small GTPases which are involved in the regulation of membrane trafficking. Mutations in this gene are associated with familial infantile myoclonic epilepsy. Alternative splicing results in multiple transcript variants.
Mutations in TBC1D24 cause                 Hereditary hearing loss            .
TBL1XR1
F-box-like/WD repeat-containing protein TBL1XR1 is a protein that in humans is encoded by the TBL1XR1 gene.
The protein encoded by this gene has sequence similarity with members of the WD40 repeat-containing protein family. The WD40 group is a large family of proteins, which appear to have a regulatory function. It is believed that the WD40 repeats mediate protein-protein interactions and members of the family are involved in signal transduction, RNA processing, gene regulation, vesicular trafficking, cytoskeletal assembly and may play a role in the control of cytotypic differentiation. Mutations in TBL1XR1 have been identified in lymphomas, including MYD88 wild-type Waldenstrom's Macroglobulinemia

# Interactions
TBL1XR1 has been shown to interact with Nuclear receptor co-repressor 1.
TIMMDC1
TIMMDC1 is a protein that in humans is encoded by the TIMMDC1 gene. It is a chaperone protein involved in constructing the membrane arm of mitochondrial Complex I. A frameshift mutation in an intron of this gene has been shown to cause failure to thrive, retardation of psychomotor development, infantile-onset hypotonia, and severe neurologic dysfunction. High expression of this gene has been associated with migration of lung cancer cells while depletion of the protein has been shown to affect regulation of apoptosis, the cell cycle, and cell migration.

# Structure
The TIMMDC1 gene is located on the q arm of chromosome 3 in position 13.33 and spans 25,760 base pairs, with 7 exons. The gene produces a 32.2 kDa protein composed of 285 amino acids. The TIMMDC1 protein has 4 transmembrane domains, with the N-terminal and C-terminal extensions localized in the mitochondrial matrix. TIMMDC1 is a multipass mitochondrial inner membrane protein, predicted to be a member of the 4-pass transmembrane protein family of TIM17-TIM22-TIM23. Its topology is predicted to be analogous to TIMM23.

# Function
TIMMDC1 is a chaperone protein involved in the assembly of the mitochondrial Complex I (NADH-ubiquinone oxidoreductase), participating in the construction of the membrane arm of complex I.

# Clinical Significance
A frameshift mutation in intron 5 of the TIMMDC1 gene has been shown to cause severe neurologic dysfunction, infantile-onset hypotonia, retardation of psychomotor development, and failure to thrive. Additionally, high expression of TIMMDC1 has been associated with metastasis of lung carcinoma cells, with depletion of the protein inhibiting growth and migration of 95D lung carcinoma cells. Depletion of TIMMDC1 has also been shown to alter expression of genes involved in the regulation of apoptosis, cell-cycle arrest, and cell migration, including CCNG2, PTEN, TIMP3, and COL3A1.

# Interactions
The TIMMDC1 protein interacts with the intermediate 315 kDa subcomplex of incompletely assembled complex I and has interactions with FATE1, in addition to about 60 other proteins. TIMMDC1 associates reciprocally with multiple components of the ECSIT-TMEM126B-ACAD9-NDUFAF1 assembly factor complex (MCIA complex).
TLQP-62
TLQP-62 (amino acid 556-617) is a VGF-derived C-terminal peptide that was first discovered by Trani et al. TLQP-62 is derived from VGF precursor protein via proteolytic cleavage by prohormone convertases PC1/3 at the RPR555 site. TLQP-62 is named after its first four N-terminal amino acids and its peptide length.

# Function
Although the receptor(s) for TLQP-62 has not been identified so far, extensive studies have demonstrated that it acts on central nervous system, peripheral nervous system and endocrine tissue to exert its biological functions.

## Synaptic plasticity
Acute TLQP-62 treatment rapidly increases synaptic activity in hippocampal neurons, and potentiates CA1 field excitatory postsynaptic potential fEPSP in the hippocampal slices, thus facilitating hippocampal synaptic transmission. TLQP-62 also increases dendritic branching and length in cultured hippocampal neurons.

## Neurogenesis
TLQP-62 treatment enhances hippocampal neurogenesis both in vitro and in vivo by promoting the proliferation in neuronal progenitor cells.

## Antidepressant efficacy
Intrahippocampal TLQP-62 infusion produces both rapid and sustained antidepressant-like effects in the forced swim test. TLQP-62's processed peptide AQEE-30, when given via intracerebroventricular route, also elicits antidepressant-like effects.

## Memory and learning
Acute intrahippocampal TLQP-62 infusion enhances memory formation via BDNF/TrkB signaling.

## Pain
Acute intrathecal administration of TLQP-62 induces hypersensitivity to mechanical and cold stimuli that recapitulates neuropathic pain, potentially by regulating the excitability of dorsal horn neurons.

## Insulin secretion
TLQP-62 treatment increases insulin secretion in cultured insulinoma cells by increasing intracellular calcium mobilization.
TMEM239
Within mammalia, TMEM239 orthologs are found in organisms belonging to eutheria and metatheria, but not prototheria. No human paralogs for TMEM239 have been identified.

# Expression
Based on human expressed sequence tag (EST) profiles, TMEM239 appears to be expressed in the testis and the brain. According to PaxDb, the abundance of TMEM239 falls within the bottom 10% relative to all other proteins in both mice and humans.  Overall, expression of TMEM239 is limited. TMEM239 appears to be expressed at moderate levels in the testes, with low expression in a variety of other tissues, including the brain and submaxillary gland.

# Interactions
TMEM239 protein interactions appear to be implicated in cell signaling, membrane transport and immunology. Human T-cell leukemia virus type-1 Protein TAX-1 (TAX) and Beta-2-microglobulin (B2M) were found to interact with TMEM239 through a host-pathogen yeast two hybrid screen.
Additional TMEM239 protein interactions were identified through a human interactome mapping project. Synthenein-1 (SDCBP) is involved in the trafficking of transmembrane proteins, in addition to neuro and immunomodulation, exosome biogenesis and tumorigenesis. SDCBP is regulated by TGFB1-mediated SMAD2/3. A number of other cell signaling proteins physically associated with TMEM239, including Cyclic AMP-dependent transcription factor (ATF-7), FYVE, RhoGEF and PH domain-containing protein 2 (FGD2) and Syndecan binding protein (SDCBP).
The Golgi SNAP receptor complex member 1 (GOS1) was found to associate with TMEM239. A member of the super-family of proteins called t-SNAREs, GOS1 mediates transport from the ER to the Golgi apparatus. Lastly, the protein Alpha-N-methyltransferease (TAE1) was found to interact with TMEM239. TAE1 catalyzes the methylation of alpha-amino groups of Alanine or Serine residues in -Pro-Lys motifs and Pro-Pro-Lys motifs. TAE1 is also responsible for methylating a number of ribosomal proteins.

# Clinical significance
SNP rs7360412, located in the 3UTR of TMEM239, was identified in a genome-wide association study of quantitative phenotypes for bipolar disorder as a top marker for fractional anisotropy. In this context, fractional anisotropy, as detected by diffusion tensor imaging, was used to assess white matter integrity. White matter integrity is highly heritable and reduced in both bipolar patients and their unaffected relatives.
RNA-seq was used to analyze the transcriptomes of human and Leishmania primary cutaneous lesions, in order to understand differences in host and parasitic factors influencing the progression of Localized Cutaneous Leishmaniasis (LCL) to Mucosal Leishmaniasis (ML). Decreased expression of TMEM239 in a primary cutaneous lesions indicates a higher probability of ML development.