FOSB

ΔFosBdelta FosBmurine osteogenic sarcoma virus
Protein fosB, also known as FosB and G0/G1 switch regulatory protein 3 (G0S3), is a protein that in humans is encoded by the FBJ murine osteosarcoma viral oncogene homolog B (FOSB) gene.wikipedia
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C-Fos

FoscFosFOS gene
The FOS gene family consists of four members: FOS, FOSB, FOSL1, and FOSL2.
It is a part of a bigger Fos family of transcription factors which includes c-Fos, FosB, Fra-1 and Fra-2.

FOSL1

fra-1
The FOS gene family consists of four members: FOS, FOSB, FOSL1, and FOSL2.
The Fos gene family consists of 4 members: c-Fos, FOSB, FOSL1, and FOSL2.

FOSL2

Fra2
The FOS gene family consists of four members: FOS, FOSB, FOSL1, and FOSL2.
The Fos gene family consists of 4 members: c-Fos, FOSB, FOSL1, and FOSL2.

Alternative splicing

alternatively splicedsplice varianttranscript variants
FosB and its truncated splice variants, ΔFosB and further truncated Δ2ΔFosB, are all involved in osteosclerosis, although Δ2ΔFosB lacks a known transactivation domain, in turn preventing it from affecting transcription through the AP-1 complex.
Overexpression of a truncated splice variant of the FOSB gene – ΔFosB – in a specific population of neurons in the nucleus accumbens has been identified as the causal mechanism involved in the induction and maintenance of an addiction to drugs and natural rewards.

Addiction

drug addictiondrug addictdrug addicts
The ΔFosB splice variant has been identified as playing a central, crucial (necessary and sufficient) role in the development and maintenance of addiction. ΔFosB overexpression (i.e., an abnormally and excessively high level of ΔFosB expression which produces a pronounced gene-related phenotype) triggers the development of addiction-related neuroplasticity throughout the reward system and produces a behavioral phenotype that is characteristic of an addiction. ΔFosB has been implicated as a critical factor in the development of virtually all forms of behavioral and drug addictions. Research on the interaction between natural and drug rewards suggests that dopaminergic psychostimulants (e.g., amphetamine) and sexual behavior act on similar biomolecular mechanisms to induce ΔFosB in the nucleus accumbens and possess bidirectional reward cross-sensitization effects that are mediated through ΔFosB.
ΔFosB, a gene transcription factor, is a critical component and common factor in the development of virtually all forms of behavioral and drug addictions.

Behavioral addiction

addictionnatural rewardaddictive
ΔFosB has been implicated as a critical factor in the development of virtually all forms of behavioral and drug addictions.
A gene transcription factor known as ΔFosB has been identified as a necessary common factor involved in both behavioral and drug addictions, which are associated with the same set of neural adaptations in the reward system.

Phencyclidine

PCPangel dustphenylcyclidine
ΔFosB overexpression has been implicated in addictions to alcohol (ethanol), cannabinoids, cocaine, methylphenidate, nicotine, opioids, phencyclidine, propofol, and substituted amphetamines, among others.
PCP is self-administered and induces ΔFosB expression in the D1-type medium spiny neurons of the nucleus accumbens, and accordingly, excessive PCP use is known to cause addiction.

Cocaine

cokecocaine traffickingcrack
ΔFosB overexpression has been implicated in addictions to alcohol (ethanol), cannabinoids, cocaine, methylphenidate, nicotine, opioids, phencyclidine, propofol, and substituted amphetamines, among others.
Cocaine addiction occurs through ΔFosB overexpression in the nucleus accumbens, which results in altered transcriptional regulation in neurons within the nucleus accumbens.

JunD

ΔJunD
These genes encode leucine zipper proteins that can dimerize with proteins of the JUN family (e.g., c-Jun, JunD), thereby forming the transcription factor complex AP-1. ΔJunD, a transcription factor, and G9a, a histone methyltransferase, both oppose the function of ΔFosB and inhibit increases in its expression.
The dominant negative mutant variant of JunD, known as ΔJunD or Delta JunD, is a potent antagonist of the ΔFosB transcript, as well as other forms of AP-1-mediated transcriptional activity.

Methylphenidate

Ritalin(RS;SR)-Methylphenidatelevomethylphenidate
ΔFosB overexpression has been implicated in addictions to alcohol (ethanol), cannabinoids, cocaine, methylphenidate, nicotine, opioids, phencyclidine, propofol, and substituted amphetamines, among others.
As with all addictive drugs, the overexpression of ΔFosB in D1-type medium spiny neurons in the nucleus accumbens is implicated in methylphenidate addiction.

Nicotine

nicotine addictionnicotine sulfateaddicted to nicotine
ΔFosB overexpression has been implicated in addictions to alcohol (ethanol), cannabinoids, cocaine, methylphenidate, nicotine, opioids, phencyclidine, propofol, and substituted amphetamines, among others.
Nicotine activates the mesolimbic pathway and induces long-term ΔFosB expression (i.e., produces phosphorylated ΔFosB isoforms) in the nucleus accumbens when inhaled or injected frequently or at high doses, but not necessarily when ingested.

Amphetamine

speedbenzedrineamphetamines
Research on the interaction between natural and drug rewards suggests that dopaminergic psychostimulants (e.g., amphetamine) and sexual behavior act on similar biomolecular mechanisms to induce ΔFosB in the nucleus accumbens and possess bidirectional reward cross-sensitization effects that are mediated through ΔFosB.
Individuals who frequently overdose on amphetamine during recreational use have a high risk of developing an amphetamine addiction, since repeated overdoses gradually increase the level of accumbal ΔFosB, a "molecular switch" and "master control protein" for addiction.

NF-κB

nuclear factor-κBNF-kappa Bnuclear factor-kappa B
The most important transcription factors that produce these alterations are ΔFosB, cyclic adenosine monophosphate (cAMP) response element binding protein (CREB), and nuclear factor kappa B (NF-κB).
NF-κB is one of several induced transcriptional targets of ΔFosB which facilitates the development and maintenance of an addiction to a stimulus.

L-DOPA

levodopa L -DOPADOPA
Dorsal striatal ΔFosB is overexpressed in rodents and primates with dyskinesias; postmortem studies of individuals with Parkinson's disease that were treated with levodopa have also observed similar dorsal striatal ΔFosB overexpression.
The longer-duration response depends on the accumulation of effects over at least two weeks, during which ΔFosB accumulates in nigrostriatal neurons. In the treatment of Parkinson's disease, this response is evident only in early therapy, as the inability of the brain to store dopamine is not yet a concern.

EHMT2

G9a
ΔJunD, a transcription factor, and G9a, a histone methyltransferase, both oppose the function of ΔFosB and inhibit increases in its expression.
G9a opposes increases in ΔFosB expression via H3K9me2 and is suppressed by ΔFosB.

Sensitization

sensitisationcentral sensitizationsensitivity
Drug sensitization occurs in drug addiction, and is defined as an increased effect of drug following repeated doses (the opposite of drug tolerance). Such sensitization involves changes in brain mesolimbic dopamine transmission, as well as a protein inside mesolimbic neurons called delta FosB. An associative process may contribute to addiction, for environmental stimuli associated with drug taking may increase craving. This process may increase the risk for relapse in addicts attempting to quit.

Levodopa-induced dyskinesia

facial and body tics are starting to manifestlevodopa-induced dyskinesiaspeak-dose dyskinesias
Viral overexpression of ΔFosB in the output neurons of the nigrostriatal dopamine pathway (i.e., the medium spiny neurons in the dorsal striatum) induces levodopa-induced dyskinesias in animal models of Parkinson's disease.
ΔFosB overexpression in the dorsal striatum (nigrostriatal dopamine pathway) via viral vectors generates levodopa-induced dyskinesia in animal models of Parkinson's disease.

Striatum

ventral striatumdorsal striatumcorpus striatum
Viral overexpression of ΔFosB in the output neurons of the nigrostriatal dopamine pathway (i.e., the medium spiny neurons in the dorsal striatum) induces levodopa-induced dyskinesias in animal models of Parkinson's disease. Transgenic mice exhibiting inducible expression of ΔFosB primarily in the nucleus accumbens and dorsal striatum exhibit sensitized behavioural responses to cocaine.
Addiction, a disorder of the brain's reward system, arises through the overexpression of delta FosB, a transcription factor, in the D1-type medium spiny neurons of the ventral striatum.

Nucleus accumbens

nucleus accumbens shellnucleus accumbens coreaccumbal
ΔFosB differs from the full length FosB and further truncated Δ2ΔFosB in its capacity to produce these effects, as only accumbal ΔFosB overexpression is associated with pathological responses to drugs.
The most important transcription factors that produce these alterations are ΔFosB, cyclic adenosine monophosphate (cAMP) response element binding protein (CREB), and nuclear factor kappa B (NFκB).

Protein

proteinsprotein synthesisproteinaceous
Protein fosB, also known as FosB and G0/G1 switch regulatory protein 3 (G0S3), is a protein that in humans is encoded by the FBJ murine osteosarcoma viral oncogene homolog B (FOSB) gene.

Gene

genesnumber of genesgene sequence
Protein fosB, also known as FosB and G0/G1 switch regulatory protein 3 (G0S3), is a protein that in humans is encoded by the FBJ murine osteosarcoma viral oncogene homolog B (FOSB) gene.

Leucine zipper

leucine zippersLeucine-zipperleucine zipper motif
These genes encode leucine zipper proteins that can dimerize with proteins of the JUN family (e.g., c-Jun, JunD), thereby forming the transcription factor complex AP-1.

Dimer (chemistry)

dimerdimerizationdimers
These genes encode leucine zipper proteins that can dimerize with proteins of the JUN family (e.g., c-Jun, JunD), thereby forming the transcription factor complex AP-1.

C-jun

JUNC-jun pathwayp39
These genes encode leucine zipper proteins that can dimerize with proteins of the JUN family (e.g., c-Jun, JunD), thereby forming the transcription factor complex AP-1.

Transcription factor

transcription factorstranscriptional factorsgene transcription factor
These genes encode leucine zipper proteins that can dimerize with proteins of the JUN family (e.g., c-Jun, JunD), thereby forming the transcription factor complex AP-1. The most important transcription factors that produce these alterations are ΔFosB, cyclic adenosine monophosphate (cAMP) response element binding protein (CREB), and nuclear factor kappa B (NF-κB).