Human Gene HNRNPLL (ENST00000409636.5) from GENCODE V44
Description: Homo sapiens heterogeneous nuclear ribonucleoprotein L like (HNRNPLL), transcript variant 2, mRNA. (from RefSeq NM_001142650) RefSeq Summary (NM_138394): HNRNPLL is a master regulator of activation-induced alternative splicing in T cells. In particular, it alters splicing of CD45 (PTPRC; MIM 151460), a tyrosine phosphatase essential for T-cell development and activation (Oberdoerffer et al., 2008 [PubMed 18669861]).[supplied by OMIM, Aug 2008]. Gencode Transcript: ENST00000409636.5 Gencode Gene: ENSG00000143889.16 Transcript (Including UTRs) Position: hg38 chr2:38,561,978-38,603,029 Size: 41,052 Total Exon Count: 14 Strand: - Coding Region Position: hg38 chr2:38,564,182-38,602,867 Size: 38,686 Coding Exon Count: 14
ID:HNRLL_HUMAN DESCRIPTION: RecName: Full=Heterogeneous nuclear ribonucleoprotein L-like; Short=hnRNPLL; AltName: Full=Stromal RNA-regulating factor; FUNCTION: RNA-binding protein that functions as regulator of alternative splicing for multiple target mRNAs, including PTPRC/CD45 and STAT5A. Required for alternative splicing of PTPRC. SUBUNIT: Interacts with HNRNPL. TISSUE SPECIFICITY: Widely expressed. Detected in bone marrow stroma cells, skeletal muscle, heart, placenta, pancreas, kidney and lung. INDUCTION: Up-regulated in stimulated T-cells. SIMILARITY: Contains 3 RRM (RNA recognition motif) domains.
The RNAfold program from the Vienna RNA Package is used to perform the secondary structure predictions and folding calculations. The estimated folding energy is in kcal/mol. The more negative the energy, the more secondary structure the RNA is likely to have.
ModBase Predicted Comparative 3D Structure on Q8WVV9
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Orthologous Genes in Other Species
Orthologies between human, mouse, and rat are computed by taking the best BLASTP hit, and filtering out non-syntenic hits. For more distant species reciprocal-best BLASTP hits are used. Note that the absence of an ortholog in the table below may reflect incomplete annotations in the other species rather than a true absence of the orthologous gene.