Persius/hicric huggingface dataset:
FOXE1
Forkhead box protein E1 is a protein that in humans is encoded by the FOXE1 gene.

# Location
The FOXE1 gene is located on the long (q) arm of chromosome 9 at position 22

# Function
This intronless gene belongs to the forkhead family of transcription factors, which is characterized by a distinct forkhead domain. This gene functions as a thyroid transcription factor which likely plays a crucial role in thyroid morphogenesis.

# Clinical significance
Mutations in this gene cause Bamforth-Lazarus syndrome and are associated with congenital hypothyroidism and cleft palate with thyroid dysgenesis. The map localization of this gene suggests it may also be a candidate gene for squamous cell epithelioma and hereditary sensory neuropathy type I.
The region surrounding the FOXE1 gene has shown association in the pathogenesis of cleft lip and palate with genome-wide levels of significance in linkage analysis studies with additional fine-mapping and replication.

# Tissue localization
FOXE1 is expressed transiently in the developing thyroid and the anterior pituitary gland.
Avian FOXE1 is also expressed in developing feathers.
FOXE3
Forkhead box protein E3 (FOXE3) also known as forkhead-related transcription factor 8 (FREAC-8) is a protein that in humans is encoded by the FOXE3 gene located on the short arm of chromosome 1.

# Function
FOXE3 is a forkhead-box transcription factor which is involved in the proper formation of the ocular lens and is post-natally expressed in the lens epithelium.

# Development
Foxe3, also known as Forkhead Box E3, is a transcription factor that is responsible for the formation of the lens placode, a precursor to the lens of the eye, and the lens itself.  Foxe3 controls multiple processes during development of the lens including, the expression of Crya which controls the solubility of the crystalline protein complex in the developing lens. Reduced solubility can lead to potential cataract formation due to crystallization of the lens. Foxe3 also controls the regulation of Prox1, which is responsible for cell cycle progression. As Foxe3 expression downregulates, Prox1 expression increases causing a reduction in cellular proliferation in the anterior lens. Foxe3 also regulates platelet-derived growth factor receptor- (Pdgfr) expression. This is responsible for lens fiber differentiation within the epithelium of certain parts of the lens. There are multiple defects associated with dysfunction of this gene with most being classified under the term anterior segment dysgenesis (ASD). For example, Peters anomaly is a rare disorder obtained during development characterized by adhesions due to malformations of the posterior corneal stroma, the absence of Descemets membrane and the corneal endothelium, and corneal opacities. This syndrome can be attributed to fetal alcohol syndrome and aneuploidy. Scientists have generated a knockout model for Foxe3 in mice and are testing the effects on the lenses of those animals. So far, it appears that Foxe3 is essential for normal lens development.

# Clinical significance
Mutations in the FOXE3 gene are  associated with anterior segment mesenchymal dysgenesis.
Homozygous mutations in this gene have been associated with a number of ocular diseases such as congenital aphakia, sclerocornea, microphthalmia, and optic disc coloboma.  There have also been reports of heterozygous mutations causing less severe ocular diseases such as anterior segment dysgenesis (sometimes referred to as anterior segment mesenchymal dysgenesis), and Peter's anomaly.
FOXG1
Forkhead box protein G1 is a protein that in humans is encoded by the FOXG1 gene.

# Function
This gene belongs to the forkhead family of transcription factors that is characterized by a distinct forkhead domain. The complete function of this gene has not yet been determined; however, it has been shown to play a role in the development of the brain and telencephalon.  Mutations of FOXG1 are the cause of FoxG1 Syndrome.

# FOXG1 syndrome
FoxG1 Syndrome is characterized by microcephaly and brain malformations. It affects most aspects of development and can cause seizures. FOXG1 syndrome is classified as an Autism Spectrum Disorder and was previously considered a variant of Rett syndrome.

# Interactions
FOXG1 has been shown to interact with JARID1B.
FOXH1
Forkhead box protein H1 is a protein that in humans is encoded by the FOXH1 gene.

# Function
FOXH1 encodes a human homolog of Xenopus forkhead activin signal transducer-1. FOXH1 protein binds SMAD2 and activates an activin response element via binding the DNA motif TGT(G/T)(T/G)ATT.

# Interactions
FOXH1 has been shown to interact with DRAP1 and Mothers against decapentaplegic homolog 2.
FOXO3
Forkhead box O3, also known as FOXO3 or FOXO3a, is a human protein encoded by the FOXO3 gene.

# Function
FOXO3 belongs to the O subclass of the forkhead family of transcription factors which are characterized by a distinct fork head DNA-binding domain. There are three other FoxO family members in humans, FOXO1, FOXO4 and FOXO6. These transcription factors share the ability to be inhibited and translocated out of the nucleus on phosphorylation by proteins such as Akt/PKB in the PI3K signaling pathway (aside from FOXO6, which may be constitutively nuclear). Other post-translational modifications including acetylation and methylation are seen and can result in increased or altered FOXO3a activity.
This protein likely functions as a trigger for apoptosis through upregulation of genes necessary for cell death, such as Bim and PUMA, or downregulation of anti-apoptotic proteins such as FLIP.
Gopinath et al.(2014) demonstrate a functional requirement for FOXO3 as a regulator of Notch signaling pathway (an essential regulator of quiescence in adult stem cells) in the self-renewal of stem cells during muscle regeneration.
It is thought that FOXO3a is also involved in protection from oxidative stress by upregulating antioxidants such as catalase and MnSOD. Ron DePinho's group generated Foxo3 knockout mice, and showed that female exhibit a dramatic age-dependent infertility, due to premature ovarian failure.

# Clinical significance
Deregulation of FOXO3a is involved in tumorigenesis, for example translocation of this gene with the MLL gene is associated with secondary acute leukemia. Downregulation of FOXO3a activity is often seen in cancer (e.g. by increase in Akt activity resulting from loss of PTEN). FOXO3 is known as a tumour suppressor.
Alternatively spliced transcript variants encoding the same protein have been observed.

# Association with longevity
A variant of FOXO3 has been shown to be associated with longevity in humans.  It is found in most centenarians across a variety of ethnic groups around the world.  The homologous genes daf-16 in the nematode C. elegans and dFOXO in the fruit fly are also associated with longevity in those organisms.
FOXP1
Forkhead box protein P1 is a protein that in humans is encoded by the FOXP1 gene. FOXP1 is necessary for the proper development of the brain, heart, and lung in mammals.  It is a member of the large FOX family of transcription factors.

# Function
This gene belongs to subfamily P of the forkhead box (FOX) transcription factor family. Forkhead box transcription factors play important roles in the regulation of tissue- and cell type-specific gene transcription during both development and adulthood. Forkhead box P1 protein contains both DNA-binding- and protein-protein binding-domains. This gene may act as a tumor suppressor as it is lost in several tumor types and maps to a chromosomal region (3p14.1) reported to contain a tumor suppressor gene(s). Alternative splicing results in multiple transcript variants encoding different isoforms.
Foxp1 is a transcription factor; specifically it is a transcriptional repressor.  Fox genes are part of a forkhead DNA-binding domain family.  This domain binds to sequences in promoters and enhancers of many genes.  Foxp1 regulates a variety of important aspects of development including tissue development of: the lungs, brain, thymus and heart.  In the heart Foxp1 has 3 vital roles, these include the regulation of cardiac myocyte maturation and proliferation, outflow tract separation of the pulmonary artery and aorta, and expression of Sox4 in cushions and myocardium.  Foxp1 is also an important gene in muscle development of the esophagus and esophageal epithelium.  Foxp1 is also an important regulator of lung airway morphogenesis. Foxp1 knockout embryos display severe defects in cardiac morphogenesis.  A few of these defects include myocyte maturation and proliferation defects that cause a thin ventricular myocardial compact zone, non-separation of the pulmonary artery and aorta, and cardiomyocyte proliferation increase and defective differentiation.  These defects, caused by Foxp1 inactivation, lead to fetal death. Disruptions of FoxP1 have been identified in very rare human patients and  similarly to FoxP2 - lead to cognitive dysfunction, including intellectual disability and autism spectrum disorder, together with language impairment.
It was shown that the embryonic stem cell (ESC)-specific isoform of FOXP1 stimulates the expression of transcription factor genes required for pluripotency, including OCT4, NANOG, NR5A2, and GDF3, while concomitantly repressing genes required for ESC differentiation. This isoform also promotes the maintenance of ESC pluripotency and contributes to efficient reprogramming of somatic cells into induced pluripotent stem cells. These results reveal a pivotal role for an Alternative splicing event in the regulation of pluripotency through the control of critical ESC-specific transcriptional programs.
The expression of FOXP1 was also implicated in the biology of B cell malignancies, and is regulated by non-coding RNA (miRNA) termed miR-150.
FSTL1
Follistatin-related protein 1 is a protein that in humans is encoded by the FSTL1 gene.

# Structure
This gene encodes a protein with similarity to follistatin, an BMP-4-binding protein. It binds to BMP-4 and TGF-1, but not Activin A. It contains an FS module (a follistatin-like sequence containing 10 conserved cysteine residues), a Kazal-type serine protease inhibitor domain, 2 EF hand domains, and a Von Willebrand factor type C domain.

# Clinical significance

## Development
FSTL1 has a role in development, such as lung development, ureter development, central nervous system development, and skeletal development.

## Arthritis
This gene product is thought to be an autoantigen associated with rheumatoid arthritis.
FSTL1 up-regulates proinflammatory mediators important in the pathology of arthritis, and serum levels of FSTL1 correlate with severity of arthritis.

## Cardiovascular diseases
FSTL1 protein seems to have a cardioprotective role.  FSTL1 attenuated hypertrophy following pressure overload and prevented myocardial ischemia/reperfusion injury in a mouse or pig model of ischemia/reperfusion. Muscle-derived Fstl1 modulates vascular remodelling in response to injury.
FSTL1 has been shown to have a pronounced ability as a possible therapeutic to stimulate regeneration following myocardial infarction.  Treating experimental animals (mouse and pig) with FSTL1 after myocardial infarction progressively restored heart function, at least in part by stimulating replication of normally non-dividing heart muscle cells
FXYD3
FXYD domain-containing ion transport regulator 3 is a protein that in humans is encoded by the FXYD3 gene.

# Function
This gene encodes a member of a family of small membrane proteins that share a 35-amino acid signature sequence domain, beginning with the sequence PFXYD and containing 7 invariant and 6 highly conserved amino acids. The approved human gene nomenclature for the family is FXYD-domain containing ion transport regulator. Mouse FXYD5 has been termed RIC (Related to Ion Channel). FXYD2, also known as the gamma subunit of the Na,K-ATPase, regulates the properties of that enzyme. FXYD1 (phospholemman), FXYD2 (gamma), FXYD3 (MAT-8), FXYD4 (CHIF), and FXYD5 (RIC) have been shown to induce channel activity in experimental expression systems. Transmembrane topology has been established for two family members (FXYD1 and FXYD2), with the N-terminus extracellular and the C-terminus on the cytoplasmic side of the membrane. The protein encoded by this gene may function as a chloride channel or as a chloride channel regulator. Two transcript variants encode two different isoforms of the protein; in addition, transcripts utilizing alternative polyA signals have been described in the literature.

# Model organisms
Model organisms have been used in the study of FXYD3 function. A conditional knockout mouse line called Fxyd3tm1a(KOMP)Wtsi was generated at the Wellcome Trust Sanger Institute. Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion. Additional screens performed:  - In-depth immunological phenotyping
FXYD5
FXYD domain-containing ion transport regulator 5 also named dysadherin (human) or RIC (mouse) is a protein that in humans is encoded by the FXYD5 gene.

# Function
This gene encodes a member of a family of small membrane proteins that share a 35-amino acid signature sequence domain, beginning with the sequence PFXYD and containing 7 invariant and 6 highly conserved amino acids. The approved human gene nomenclature for the family is FXYD-domain containing ion transport regulator. Mouse FXYD5 has been termed RIC (Related to Ion Channel). FXYD2, also known as the gamma subunit of the Na,K-ATPase, regulates the properties of that enzyme. FXYD1 (phospholemman), FXYD2 (gamma), FXYD3 (MAT-8), FXYD4 (CHIF), and FXYD5 (RIC) have been shown to induce channel activity in experimental expression systems. Transmembrane topology has been established for two family members (FXYD1 and FXYD2), with the N-terminus extracellular and the C-terminus on the cytoplasmic side of the membrane. This gene product, FXYD5, has not been characterized as a protein. Two transcript variants have been found for this gene, and they are both predicted to encode the same protein.
Dysadherin is the gamma5 subunit the human Na,K-ATPase. Of all the FXYD members, dysadherin is the only member that has a large extracellular sequence of 140 amino acids. Dysadherin has been observed to be over-expressed on the surface of cells that have down regulated levels of surface E-cadherin. CCL2 (bone homing cytokine)is a protein that is highly affected by silencing dysadherin expression. Dysadherin interferes with cell adhesion via beta1 subunit interactions. Dysdaherin is a target for an extracellular antibody drug conjugate where the antibody to dysadherin is attached to a cardiac glycoside.

# Clinical significance
Dysadherin has been found to be a marker for metastatic cancers and found up-regulated in multiple cancer types.
FXYD6
FXYD6 (pronounced fix-id six), or FXYD domain-containing ion transport regulator 6, is a gene which is located at the 11q23.3 (chromosome 11 locus 23.3).  The FXYD6 protein contains 95 amino acids, and can be found in all human tissues except blood.
This gene belongs to the FXYD family of ion transport regulators 

# Pathology
According to recent research, mutations in the FXYD6 gene, or in sequences close by this gene, can predispose to the schizophrenia which is known to be strongly heritable.
Femur
In humans, it is the longest, most voluminous, and strongest bone. The average human femur is 48 centimeters (19 in) in length and 2.34 cm (0.92 in) in diameter and can support up to 30 times the weight of an adult. It forms part of the hip (at the acetabulum) and part of the knee.
The word femur is Latin for thigh. Theoretically in strict usage, femur bone is more proper than femur, as in classical Latin femur means "thigh", and os femoris means "the bone within it".
In medical Latin its genitive is always femoris, but in classical Latin its genitive is often feminis, and should not be confused with case forms of femina, which means "woman".

# Fractures
Femur bone fractures, on occasion, are liable to cause permanent disability because the thigh muscles pull the fragments so they overlap, and the fragments re-unite incorrectly. To avoid this, femur fracture patients should be put into traction to keep the fragments pulled into proper alignment.
With modern medical procedures, such as the insertion of rods and screws by way of surgery (known as Antegrade  or Retrograde  femoral rodding), those suffering from femur fractures can now generally expect to make a full recovery, though one that generally takes 3 to 6 months due to the bone's size. Patients should not put weight on the leg without permission from an orthopedic surgeon since this can delay the healing process.
The thigh is generally not put in a cast since the surgical hardware does the job of straightening the bone and holding the fracture together while it heals. Permanent complications with this procedure include the risk of intra-articular sepsis, arthritis and knee stiffness. After the bone is healed, there is no further need for the hardware but, while it is left in some patients permanently, those who lead an active lifesytle may experience discomfort where the hardware projects into the leg muscle and, in such cases, the hardware can be removed, most commonly by means of out-patient surgery.

## Hip fracture
If bone is weakened, the proximal end of the femur bone near the hip joint is prone to fragility fracture.  Most at risk are European descent, post-menopausal women, and osteoporosis severely increases this risk. Out of all the bones in the skeleton, the femur takes the longest to heal. This bone is the longest and strongest bone in the human body. When the average human being jumps this bone withstands a force of half a ton just a testament to its strength.

# Intercondylar Fossa
The intercondylar fossa is present between the condyles at the distal end of the femur. In addition to the intercondylar eminence on the tibial plateau, there is both an anterior and posterior intercondylar fossa (area), the sites of anterior cruciate and posterior cruciate ligament attachment, respectively.

# In other animals
Parallel structures by the same name exist in other complex animals, such as the bone inside a ham or a leg of lamb. The name femur is also given to the most proximal full-length jointed segment of an arthropod's leg.
Fluid

# Overview
A fluid is defined as a substance that continually deforms (flows) under an applied shear stress regardless of how small the applied stress. All liquids and all gases are fluids. Fluids are a subset of the phases of matter and include liquids, gases, plasmas and, to some extent, plastic solids.
Liquids form a free surface (that is, a surface not created by the container) while gases do not. The distinction between solids and fluids is not entirely obvious. The distinction is made by evaluating the viscosity of the substance.  Silly Putty can be considered either a solid or a fluid, depending on the time period over which it is observed.
Fluids display such properties as:
- not resisting deformation, or resisting it only lightly (viscosity), and
- the ability to flow (also described as the ability to take on the shape of the container).
These properties are typically a function of their inability to support a shear stress in static equilibrium.
Solids can be subjected to shear stresses, and to normal stresses - both compressive and tensile.  In contrast, ideal fluids can only be subjected to normal, compressive stress which is called pressure.  Real fluids display viscosity and so are capable of being subjected to low levels of shear stress.
In a solid, shear stress is a function of strain, but in a fluid, shear stress is a function of rate of strain. A consequence of this behavior is Pascal's law which describes the role of pressure in characterizing a fluid's state.
Depending on the relationship between shear stress, and the rate of strain and its derivatives, fluids can be characterized as:
- Newtonian fluids : where stress is directly proportional to rate of strain, and
- Non-Newtonian fluids : where stress is proportional to rate of strain, its higher powers and derivatives.
The behavior of fluids can be described by the Navier-Stokes equations - a set of partial differential equations which are based on:
- continuity (conservation of mass),
- conservation of linear momentum
- conservation of angular momentum
- conservation of energy.
The study of fluids is fluid mechanics, which is subdivided into fluid dynamics and fluid statics depending on whether the fluid is in motion.
GLUT5
GLUT5 is a fructose transporter expressed on the apical border of enterocytes in the small intestine. GLUT5 allows for fructose to be transported from the intestinal lumen into the enterocyte by facilitated diffusion due to fructose's high concentration in the intestinal lumen. GLUT5 is also expressed in skeletal muscle, testis, kidney, fat tissue (adipocytes), and brain.
Fructose malabsorption or Dietary Fructose Intolerance is a dietary disability of the small intestine, where the amount of fructose carrier in enterocytes is deficient.
In humans the GLUT5 protein is encoded by the SLC2A5 gene.

# Regulation
Fructose uptake rate by GLUT5 is significantly affected by diabetes mellitus, hypertension, obesity, fructose malabsorption, and inflammation. However, age-related changes in fructose intake capability are not explained by the rate of expression of GLUT5. The absorption of fructose in the simultaneous presence of glucose is improved, while sorbitol is inhibitory.

# Interactive pathway map
Click on genes, proteins and metabolites below to link to respective articles. 
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