======= MAGEL2 =======


== Gene Information ==
  * **<color #00a2e8>Official Symbol</color>**: MAGEL2
  * **<color #00a2e8>Official Name</color>**: MAGE family member L2
  * **<color #00a2e8>Aliases and Previous Symbols</color>**: N/A
  * **<color #00a2e8>Entrez ID</color>**: [[https://www.ncbi.nlm.nih.gov/gene/?term=54551|54551]]
  * **<color #00a2e8>UniProt</color>**: [[https://www.uniprot.org/uniprot/Q9UJ55|Q9UJ55]]
  * **<color #00a2e8>Interactions</color>**: [[https://thebiogrid.org/search.php?search=MAGEL2&organism=9606|BioGRID]]
  * **<color #00a2e8>PubMed articles</color>**: [[https://www.ncbi.nlm.nih.gov/pubmed/?term=gene%20MAGEL2|Open PubMed]]
  * **<color #00a2e8>OMIM</color>**: [[https://omim.org/entry/605283|Open OMIM]]

== Function Summary ==
  * **<color #00a2e8>Entrez Summary</color>**:  Prader-Willi syndrome (PWS) is caused by the loss of expression of imprinted genes in chromosome 15q11-q13 region. Affected individuals exhibit neonatal hypotonia, developmental delay, and childhood-onset obesity. Necdin (NDN), a gene involved in the terminal differentiation of neurons, localizes to this region of the genome and has been implicated as one of the genes responsible for the etiology of PWS. This gene is structurally similar to NDN, is also localized to the PWS chromosomal region, and is paternally imprinted, suggesting a possible role for it in PWS. [provided by RefSeq, Oct 2010]. 
  * **<color #00a2e8>UniProt Summary</color>**:  Probably enhances ubiquitin ligase activity of RING-type zinc finger-containing E3 ubiquitin-protein ligases, possibly through recruitment and/or stabilization of the Ubl-conjugating enzyme (E2) at the E3:substrate complex. Acts as a regulator of retrograde transport via its interaction with VPS35. Recruited to retromer-containing endosomes and promotes the formation of 'Lys- 63'-linked polyubiquitin chains at 'Lys-220' of WASHC1 together with TRIM27, leading to promote endosomal F-actin assembly (PubMed:23452853). Regulates the circadian clock by repressing the transcriptional activator activity of the CLOCK-ARNTL/BMAL1 heterodimer. Significantly promotes the cytoplasmic accumulation of CLOCK (By similarity). {ECO:0000250|UniProtKB:Q9QZ04, ECO:0000269|PubMed:20864041, ECO:0000269|PubMed:23452853}.

<button type='primary' size='sm' modal='Pfam_Domains'>Pfam Domains</button>
<button type='primary' size='sm' modal='GO_terms'>GO Terms</button>


<modal id='Pfam_Domains' size='lg' title='Pfam Domains'>
|MAGE|
</modal>

<modal id='GO_terms' size='lg' title='GO Terms'>
|positive regulation of actin nucleation|
|retromer complex|
|Arp2/3 complex-mediated actin nucleation|
|regulation of actin nucleation|
|actin nucleation|
|protein K63-linked ubiquitination|
|positive regulation of actin filament polymerization|
|retrograde transport, endosome to Golgi|
|regulation of circadian rhythm|
|positive regulation of protein polymerization|
|cytosolic transport|
|regulation of actin filament polymerization|
|regulation of actin polymerization or depolymerization|
|regulation of actin filament length|
|positive regulation of supramolecular fiber organization|
|positive regulation of cytoskeleton organization|
|regulation of protein polymerization|
|endosomal transport|
|actin filament organization|
|ubiquitin-protein transferase activity|
|positive regulation of protein complex assembly|
|early endosome|
|regulation of actin filament organization|
|endosome|
|rhythmic process|
|protein polyubiquitination|
|regulation of actin cytoskeleton organization|
|regulation of supramolecular fiber organization|
|regulation of cellular component size|
|regulation of actin filament-based process|
|regulation of protein complex assembly|
|supramolecular fiber organization|
|actin cytoskeleton organization|
|regulation of anatomical structure size|
|positive regulation of cellular component biogenesis|
|regulation of cytoskeleton organization|
|actin filament-based process|
|positive regulation of organelle organization|
|protein ubiquitination|
|protein modification by small protein conjugation|
|regulation of cellular component biogenesis|
|protein modification by small protein conjugation or removal|
|cytoskeleton organization|
|negative regulation of transcription, DNA-templated|
|positive regulation of cellular component organization|
|negative regulation of nucleic acid-templated transcription|
|negative regulation of RNA biosynthetic process|
|regulation of organelle organization|
|negative regulation of RNA metabolic process|
|negative regulation of cellular macromolecule biosynthetic process|
|negative regulation of nucleobase-containing compound metabolic process|
|negative regulation of macromolecule biosynthetic process|
|negative regulation of cellular biosynthetic process|
|intracellular transport|
|negative regulation of biosynthetic process|
|negative regulation of gene expression|
|establishment of localization in cell|
|vesicle-mediated transport|
</modal>
\\

 === CRISPR Data ===
<button type='default' size='small' modal='Compound_Hit'>Compound Hit</button>
<button type='default' size='small' modal='Most_Correlated_Genes'>Most Correlated Genes in Chemogenomics</button>
<button type='primary' size='small' modal='Essential_Avana'>Tissues where Essential in the Avana Dataset (DepMap 20Q1)</button>

<modal id='Compound_Hit' size='lg' title='Compound Hit'>
No hits were found.
</modal>

<modal id='Most_Correlated_Genes' size='lg' title='Most Correlated Genes in Chemogenomics'>
No correlation found to any other genes in chemogenomics.
</modal>

<modal id='Essential_Avana' size='lg' title='Tissues where Essential in the Avana Dataset (DepMap 20Q1)'>
Global Fraction of Cell Lines Where Essential: N/A
^Tissue^Fraction Of Cell Lines Where Essential^
</modal>

== Essentiality in NALM6  ==
    * **<color #00a2e8>Essentiality Rank</color>**: 6563
    * **<color #00a2e8>Expression level (log2 read counts)</color>**: -2.9 
<button type='primary' size='small' modal='Dist_expr'>Expression Distribution</button>
<modal id='Dist_expr' size='lg' title='MAGEL2 Expression in NALM6 Cells: -2.9'>
{{:chemogenomics:nalm6 dist.png?nolink |}}
</modal>