Persius/hicric huggingface dataset:
LMO4
LIM domain transcription factor LMO4 is a protein that in humans is encoded by the LMO4 gene.
LIM domain only 4 is a cysteine-rich, two LIM domain-containing protein that may play a role as a transcriptional regulator or possibly an oncogene.  Its mRNA is characterized by a GC-rich 5' region and by multiple ATTT motifs in the 3' region.  A variant transcript missing a portion of the 5' region has been identified but cannot be confirmed because of the GC-rich nature of the region.

# Interactions
LMO4 has been shown to interact with LDB1, RBBP8 and BRCA1.
LQT4

# Overview
The LTQ4 subtype of long QT syndrome is caused by a mutation in the genes which code for proteins cause ankyrins. People with this mutation experience sinus bradycardia, junctional escape rhythms, atrial fibrillation, and sudden death after physical or emotional stress. Ankyrins are important proteins that bind to various types of vital cell membrane channels which regulate the concentration of intracellular electrolytes. Abnormalities in the channels as a result of defective ankyrin proteins can lead to dangerous levels of intracellular calcium, and fatal arrhythmias. LQT4 is the only subtype of LQTS that does not involve sudden cardiac death as a part of another genetic disorder called Rett syndrome.

# LQT4 Subtype

## Genetics and Pathophysiology
The LQT4 genes are ANK2 and ANKB which are located on chromosome 4q25-27 , and code for proteins called ankyrins. They are proteins which affect the function of several important ion channel proteins such as the chloride-bicarbonate anion exchanger, ATPase, calcium release channels, and the voltage gated sodium channel. The proteins physically link the lipid bilayer of the cell membrane to the skeleton of the membrane. A mutation in the LTQ4 genes that code for ankyrins can cause increased intracellular concentrations of calcium, and can therefore cause fatal arrhythmias. People with this mutation experience sinus bradycardia, junctional escape rhythms, atrial fibrillation, and sudden death after physical or emotional stress has also been known to occur.

## History and Symptoms
- Seizures - due to oxygen deprivation that occurs during arrhythmia.
- Fainting - fainting or syncope is the most common symptom LQTS.
- A prodrome may occur before losing consciousness, which may consist of lightheadedness, heart palpitations, blurred vision or weakness.
- Sudden death - a fatal arrhythmia that is not quickly intervened on, may cause sudden death.
- In LQT4, events may particularly occur after physical or emotional stress.

## Therapy
- Beta-blockers are the first line treatment in LQTS, even in asymptomatic carriers, as they reduce the incidence of syncope and sudden cardiac death.
- Other medications to control non-malignant arrhythmias.
- Electrolytes should be repleted as neccesary.
- Avoidance of triggers (drugs, supplements, loud noises, exercise).
- LQTs is one of the few diseases where genetic testing can provide important guidance, such as in whom to place an AICD (defibrillator) for the primary prevention of cardiac events. 
- Placement of a pacemaker may be indicated.
- Left stellectomy is not a cure, but is a second line therapy to reduce the risk of sudden cardiac death and is indicated if the patient does not tolerate beta blockers, as well as in young patients under the age of 12 where beta blockers are not deemed protective enough and AICD is not appropriate.
- Patients with long QT syndrome should undergo secondary prevention with AICD implantation if they sustain an aborted cardiac arrest or sudden cardiac death.
LQT5

# Overview
LQT5 subtype of long QT syndrome is an autosomal dominant mutation that leads to a defect in the potassium channel. In its rare homozygous form it can cause Jervell and Lange-Nielsen syndrome.

# LQT5 Subtype

## Genetics and Pathophysiology
LQT5 is an autosomal dominant relatively uncommon form of LQTS. It involves mutations in the gene KCNE1 which encodes for the potassium channel beta subunit MinK. In its rare homozygous forms it can lead to Jervell and Lange-Nielsen syndrome. As in LQT1, LQT5 can lead to a decreased excretion of potassium from the cell and will show prolongation of the QT interval on EKG.

## History and Symptoms
- Seizures - due to oxygen deprivation that occurs during arrhythmia.
- Fainting - fainting or syncope is the most common symptom LQTS.
- A prodrome may occur before losing consciousness, which may consist of lightheadedness, heart palpitations, blurred vision or weakness.
- Sudden death - a fatal arrhythmia that is not quickly intervened on, may cause sudden death.
- History of sensorineural deafness as occurs in Jervell and Lange-Nielsen syndrome.

## Therapy
- Beta-blockers are the first line treatment in LQTS, even in asymptomatic carriers, as they reduce the incidence of syncope and sudden cardiac death.
- Other medications to control non-malignant arrhythmias.
- Electrolytes should be repleted as neccesary.
- Avoidance of triggers (drugs, supplements, loud noises, exercise).
- LQTs is one of the few diseases where genetic testing can provide important guidance, such as in whom to place an AICD (defibrillator) for the primary prevention of cardiac events. 
- Placement of a pacemaker may be indicated.
- Left stellectomy is not a cure, but is a second line therapy to reduce the risk of sudden cardiac death and is indicated if the patient does not tolerate beta blockers, as well as in young patients under the age of 12 where beta blockers are not deemed protective enough and AICD is not appropriate.
- Patients with long QT syndrome should undergo secondary prevention with AICD implantation if they sustain an aborted cardiac arrest or sudden cardiac death.
LQT6

# Overview
LQT6 is a rare form of long QT syndrome.

# LQT6 Subtype
LQT6 is an autosomal dominant relatively uncommon form of LQTS. It involves mutations in the gene KCNE2 which encodes for the potassium channel beta subunit MiRP1, constituting part of the IKr repolarizing K+ current.

## History and Symptoms
- Seizures - due to oxygen deprivation that occurs during arrhythmia.
- Fainting - fainting or syncope is the most common symptom LQTS.
- A prodrome may occur before losing consciousness, which may consist of lightheadedness, heart palpitations, blurred vision or weakness.
- Sudden death - a fatal arrhythmia that is not quickly intervened on, may cause sudden death.

## Therapy
- Beta-blockers are the first line treatment in LQTS, even in asymptomatic carriers, as they reduce the incidence of syncope and sudden cardiac death.
- Other medications to control non-malignant arrhythmias.
- Electrolytes should be repleted as neccesary.
- Avoidance of triggers (drugs, supplements, loud noises, exercise).
- LQTs is one of the few diseases where genetic testing can provide important guidance, such as in whom to place an AICD (defibrillator) for the primary prevention of cardiac events. 
- Placement of a pacemaker may be indicated.
- Left stellectomy is not a cure, but is a second line therapy to reduce the risk of sudden cardiac death and is indicated if the patient does not tolerate beta blockers, as well as in young patients under the age of 12 where beta blockers are not deemed protective enough and AICD is not appropriate.
- Patients with long QT syndrome should undergo secondary prevention with AICD implantation if they sustain an aborted cardiac arrest or sudden cardiac death.
LQT8

# Overview
LQT8 subtype of long QT syndrome, also known as Timothy's syndrome is due to mutations causing abnormalities in calcium channels. LQT8 is associated with the finding of syndactyly.

# LQT8 Subtype
Timothy's syndrome is due to mutations in the calcium channel Cav1.2 encoded by the gene CACNA1c. Since the Calcium channel Cav1.2 is abundant in many tissues, patients with Timothy's syndrome have many clinical manifestations including congenital heart disease, autism, syndactyly and immune deficiency.

## History and Symptoms
- Seizures - due to oxygen deprivation that occurs during arrhythmia.
- Fainting - fainting or syncope is the most common symptom LQTS.
- A prodrome may occur before losing consciousness, which may consist of lightheadedness, heart palpitations, blurred vision or weakness.
- Sudden death - a fatal arrhythmia that is not quickly intervened on, may cause sudden death.

## Physical Exam
- Physical exam may show syndactyly.

## Therapy
- Beta-blockers are the first line treatment in LQTS, even in asymptomatic carriers, as they reduce the incidence of syncope and sudden cardiac death.
- Other medications to control non-malignant arrhythmias.
- Electrolytes should be repleted as neccesary.
- Avoidance of triggers (drugs, supplements, loud noises, exercise).
- LQTs is one of the few diseases where genetic testing can provide important guidance, such as in whom to place an AICD (defibrillator) for the primary prevention of cardiac events. 
- Placement of a pacemaker may be indicated.
- Left stellectomy is not a cure, but is a second line therapy to reduce the risk of sudden cardiac death and is indicated if the patient does not tolerate beta blockers, as well as in young patients under the age of 12 where beta blockers are not deemed protective enough and AICD is not appropriate.
- Patients with long QT syndrome should undergo secondary prevention with AICD implantation if they sustain an aborted cardiac arrest or sudden cardiac death.
LQT9

# Overview
LQT9 subtype is a variant of long QT syndrome, which causes abnormalities in a membrane protein called caveolin.

# LQT9
This newly discovered variant is caused by mutations in the membrane structural protein,caveolin-3.  Caveolins form specific membrane domains called caveolae in which among others the NaV1.5 voltage-gated sodium channel sits.   Similar to LQT3, these particular mutations increase so-called 'late' sodium current which impairs cellular repolarization.

## History and Symptoms
- Seizures - due to oxygen deprivation that occurs during arrhythmia.
- Fainting - fainting or syncope is the most common symptom LQTS.
- A prodrome may occur before losing consciousness, which may consist of lightheadedness, heart palpitations, blurred vision or weakness.
- Sudden death - a fatal arrhythmia that is not quickly intervened on, may cause sudden death.

## Therapy
- Beta-blockers are the first line treatment in LQTS, even in asymptomatic carriers, as they reduce the incidence of syncope and sudden cardiac death.
- Other medications to control non-malignant arrhythmias.
- Electrolytes should be repleted as neccesary.
- Avoidance of triggers (drugs, supplements, loud noises, exercise).
- LQTs is one of the few diseases where genetic testing can provide important guidance, such as in whom to place an AICD (defibrillator) for the primary prevention of cardiac events. 
- Placement of a pacemaker may be indicated.
- Left stellectomy is not a cure, but is a second line therapy to reduce the risk of sudden cardiac death and is indicated if the patient does not tolerate beta blockers, as well as in young patients under the age of 12 where beta blockers are not deemed protective enough and AICD is not appropriate.
- Patients with long QT syndrome should undergo secondary prevention with AICD implantation if they sustain an aborted cardiac arrest or sudden cardiac death.
LRBA
Lipopolysaccharide-responsive and beige-like anchor protein is a protein that in humans is encoded by the LRBA gene.
Patients with Chediak-Higashi syndrome (CHS1; MIM 214500) suffer from a systemic immunodeficiency involving defects in polarized trafficking of vesicles in a number of immune system cell types. In mouse, this syndrome is reproduced in strains with a mutation in the 'beige' gene that results in proteins lacking the BEACH (beige and CHS1) domain and C-terminal WD repeats. LRBA contains key features of both beige/CHS1 and A kinase anchor proteins (AKAPs; see MIM 602449).
Deficiency of this protein in humans causes the codntion known as LPS-responsive beige-like anchor protein deficiency.
LRG1
Leucine-rich alpha-2-glycoprotein 1 is a protein which in humans is encoded by the  gene LRG1.

# Function
The leucine-rich repeat (LRR) family of proteins, including LRG1, have been shown to be involved in protein-protein interaction, signal transduction, and cell adhesion and development. LRG1 is expressed during granulocyte differentiation.
LRG1 has been shown to be involved in promoting neovascularization (new blood vessel growth) through causing a switch in transforming growth factor beta (TGFbeta) signaling in endothelial cells. LRG1 binds to the accessory receptor endoglin and promotes signaling via the ALK1-Smad1/5/8 pathway.

# Application
Levels of the LRG protein are markedly elevated in acute appendicitis and therefore could be used as a diagnostic aid.
LRG1 may be a potential therapeutifc target for the treatment of diseases where there is aberrant neovascularization.
LRP2
Low density lipoprotein-related protein 2 also known as LRP2 or megalin is a protein which in humans is encoded by the LRP2 gene.

# Function
LRP2 was identified as the antigen of rat experimental membranous nephropathy (Heyman nephritis) and originally named gp330  and subsequently megalin and later LRP2. LRP2/megalin is a multiligand binding receptor found in the plasma membrane of many absorptive epithelial cells.  LRP2/megalin is a member of a family of receptors with structural similarities to the low density lipoprotein receptor (LDLR). LRP2/megalin functions to mediate endocytosis of ligands leading to degradation in lysosomes or transcytosis. LRP2/megalin can also form complexes with cubilin: those complexes are able to reabsorb several molecules and can be inhibited by sodium maleate.
LRP2 is expressed in epithelial cells of the thyroid (thyrocytes), where it can serve as a receptor for the protein thyroglobulin (Tg).

# Clinical significance
Mutations in the LRP2 gene are associated with Donnai-Barrow syndrome.

# Interactions
LRP2 has been shown to interact with:
- DAB2,
- DLG4,
- GIPC1,
- ITGB1BP1,
- LDL-receptor-related protein associated protein,
- LDLRAP1,
- MAGI1,
- MAPK8IP1,
- MAPK8IP2,
- NOS1AP,  and
- SYNJ2BP.
LRP6
Low-density lipoprotein receptor-related protein 6 is a protein that in humans is encoded by the LRP6 gene. LRP6 is a key component of the LRP5/LRP6/Frizzled co-receptor group that is involved in canonical Wnt pathway.

# Structure
LRP6 is a transmembrane low-density lipoprotein receptor that shares a similar structure with LRP5. In each protein, about 85% of its 1600-amino-acid length is extracellular. Each has four -propeller motifs at the amino terminal end that alternate with four epidermal growth factor (EGF)-like repeats. Most extracellular ligands bind to LRP5 and LRP6 at the -propellers. Each protein has a single-pass, 22-amino-acid segment that crosses the cell membrane and a 207-amino-acid segment that is internal to the cell.

# Function
LRP6 acts as a co-receptor with LRP5 and the Frizzled protein family members for transducing signals by Wnt proteins through the canonical Wnt pathway.

# Interactions
Canonical WNT signals are transduced through Frizzled receptor and LRP5/LRP6 coreceptor to downregulate GSK3beta (GSK3B) activity not depending on Ser-9 phosphorylation. Reduction of canonical Wnt signals upon depletion of LRP5 and LRP6 results in p120-catenin degradation.
LRP6 is regulated by extracellular proteins in the Dickkopf (Dkk) family (like DKK1), sclerostin, R-spondins and members of the cysteine-knot-type protein family.

# Clinical significance
Loss-of-function mutations or LRP6 in humans lead to increased plasma LDL and triglycerides, hypertension, diabetes and osteoporosis. Similarly, mice with a loss-of-function Lrp6 mutation have low bone mass. LRP6 is critical in bone's anabolic response to parathyroid hormone (PTH) treatment, whereas LRP5 is not involved. On the other hand, LRP6 does not appear active in mechanotransduction (bone's response to forces), while LRP5 is critical in that role. 
Sclerostin, one of the inhibitors of LRP6, is a promising osteocyte-specific Wnt antagonist in osteoporosis clinical trials.
LSM2
U6 snRNA-associated Sm-like protein LSm2 is a protein that in humans is encoded by the LSM2 gene.

# Function
Sm-like proteins were identified in a variety of organisms based on sequence homology with the Sm protein family (see SNRPD2; MIM 601061). Sm-like proteins contain the Sm sequence motif, which consists of 2 regions separated by a linker of variable length that folds as a loop. The Sm-like proteins are thought to form a stable heteromer present in tri-snRNP particles, which are important for pre-mRNA splicing.

# Interactions
LSM2 has been shown to interact with DDX20, LSM3, LSM8 and LSM7.
LYK5
Protein kinase LYK5, also known as LYK5 or STRAD, is a human protein and also denotes the gene encoding it.

# Function
Endogenous LKB1 and STRAD form a complex in which STRAD activates LKB1, resulting in phosphorylation of both partners. Removal of endogenous LYK5 by small interfering RNA abrogates LKB1-induced G1 phase arrest. STRAD stabilizes LKB1 protein both in vivo and in vitro, and is capable of eliciting multiple axons in mouse embryonic cortical cultured neurons when overexpressed with LKB1. STRAD is highly spliced in vivo, and this is both developmentally regulated and tissue-specific, but the unique functions of the splice variants are not yet understood.

# Disease linkage
Mutations in the LYK5/STRAD gene are associated with polyhydramnios, megalencephaly and symptomatic epilepsy (collectively known as the PMSE syndrome).

# Interactions
STRAD has been shown to interact with LKB1 and MO25.
Lisp

# Background
A lisp (O E wlisp, stammering) is a speech impediment, historically also known as sigmatism. Stereotypically, people with a lisp are unable to pronounce sibilants (like the sound ]), and replace them with interdentals (like the sound ]), though there are actually several kinds of lisp. The result is that the speech is unclear.
- "Interdental" lisping is produced when the tip of the tongue protrudes between the front teeth and "dentalised" lisping is produced when the tip of the tongue just touches the front teeth.
- The "lateral" lisp, where the Template:IPA and Template:IPA sounds are produced with air escaping over the sides of the tongue, is also called 'slushy ess' or a 'slushy lisp' due to the wet, spitty sound. The symbols for these lateralized sounds are in the Extended International Phonetic Alphabet for speech disorders, Template:IPA and Template:IPA.
- Finally there is the "palatal lisp" where the speaker attempts to make the sounds with the tongue in contact with the palate.
Lust
Lust is any intense desire or craving for gratification and excitement.  Lust can mean strictly sexual lust, although it is also common to speak of a "lust for men", "lust for blood (bloodlust for short)" or a "lust for power", or other goals and to "lust for love". The Greek word which translates as lust is epithymia (), which also is translated into English as "to covet".

# Lust in the context of religion

## ChristianityGeneral
Catholic tradition considers lust to be one of the main sins or vices. In the Old Testament, adultery was punishable by stoning. In the New Testament, Jesus included looking "lustfully at a woman" as adultery. (Matthew 5:28)
The "woman" is a "Married" woman.

## ChristianityProtestantism
Protestants hold that all sins, including lust, can be forgiven only by God through the death and resurrection of Jesus Christ. If a person believes in Jesus as his only Savior, then that person, regardless of what he has done, will receive Jesus' righteousness and will be able to enter heaven. But to enter the heaven of God , One must receive the Spirit of God . The Holy Bible tells of this in Luke 7:36-50, where the Lord Jesus Christ forgives a sinful woman.

## Punishment in the afterlife
According to some Christian sources , reprobates whose chief unforgiven sin is lust are punished in Hell by being "smothered in fire and brimstone." However, while most Christian traditions agree that at some point after death the damned individuals find themselves in a hell where they suffer punishment for their sins, most traditions also agree that one can only speculate regarding the precise nature of any punishment above and beyond the principal torment, which comes simply from being totally separated from God.
In Dante's Inferno, the first Canticle of the Divine Comedy, the lustful are punished by being continuously swept around in a whirlwind, which symbolizes their passions.

## Repentance in Purgatory
According to The Divine Comedy, penitents who are guilty of lust cleanse their soul of the sin by walking through flames, thereby purging their minds of all lustful thoughts.

## Judaism
According to traditional Judaism, nothing on Earth was created without a purpose. This includes basic human drives. Lust is only sinful when it is after another man's possessions or wife. Lust is not only not sinful, but a mitzvah, when one lusts after their spouse.

## Symbolic representations
A frequent visual symbol for the sin of lust is the color blue, as with the cover of the book Lust in The Seven Deadly Sins series published by the Oxford University Press.
Another symbol of lust is the animal cow (or bull). An example of this appears in the engraving Shamelessness  by the 16th century artist Georg Pencz.
Also, lust can be seen in the eponymous Eighth ATU in the Thoth Tarot card of Aleister Crowley.
MAP4
Microtubule-associated protein 4 is a protein that in humans is encoded by the MAP4 gene.
The protein encoded by this gene is a major non-neuronal microtubule-associated protein. This protein contains a domain similar to the microtubule-binding domains of neuronal microtubule-associated protein (MAP2) and microtubule-associated protein tau (MAPT/TAU). This protein promotes microtubule assembly, and has been shown to counteract destabilization of interphase microtubule catastrophe promotion. Cyclin B was found to interact with this protein, which targets cell division cycle 2 (CDC2) kinase to microtubules. The phosphorylation of this protein affects microtubule properties and cell cycle progression. Multiple alternatively spliced transcript variants encoding distinct isoforms have been observed, the full-length nature of three of which are supported.
uMAP4, the ubiquitous isoform of MAP4, functions in the architecture and positioning of the mitotic spindle in human cells. oMAP4 is predominantly expressed in brain and muscle and has been shown to organise microtubules into antiparallel bundles. mMAP4 is a muscle-specific isoform.
MAS1
MAS proto-oncogene, or MAS1 proto-oncogene, G protein-coupled receptor (MRGA,MAS,MGRA""), is a protein that in humans is encoded by the MAS1 gene.
The structure of the MAS1 product indicates that it belongs to the class of receptors that are coupled to GTP-binding proteins and share a conserved structural motif, which is described as a '7-transmembrane segment' following the prediction that these hydrophobic segments form membrane-spanning alpha-helices. The MAS1 protein may be a receptor that, when activated, modulates a critical component in a growth-regulating pathway to bring about oncogenic effects.
Agonists of the receptor include angiotensin-(1-7). Antagonist include A-779 (angiotensin-1-7 with c-terminal proline substituted for D-Ala), or D-Pro (angiotensin-1-7 with c-terminal proline submitted for D-proline).
Mas1 proto-oncogene (MAS1, MGRA) is not to be confused with the MAS-related G-protein coupled receptor, a recently believed to be activated by the ligand alamandine (generated by catalysis of Ang A via ACE2 or directly from Ang-(1-7)).