Proteins LRRTM2, Human
- Known as:
- Proteins LRRTM2, Human
- Catalog number:
- C618
- Product Quantity:
- 10μg
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Proteins LRRTM2 Human
Related genes to: Proteins LRRTM2, Human
- Gene:
- LRRTM2 NIH gene
- Name:
- leucine rich repeat transmembrane neuronal 2
- Previous symbol:
- -
- Synonyms:
- KIAA0416
- Chromosome:
- 5q31.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-06-22
- Date modifiied:
- 2016-10-25
Related products to: Proteins LRRTM2, Human
Related articles to: Proteins LRRTM2, Human
- Precise establishment of distinct cerebral cortex circuits is essential for sensorimotor function, high-level cognition, and cross-modality integration and association. Although an increasing set of molecular controls over subtype-specific cortical wiring have been identified, much less is known about how molecules in growth cones (GCs) regulate precise long-range projection of axons through complex environments, or how dysregulation of GC molecular machinery disrupts precision of circuit formation. Here, we discover a generalizable mechanism for regulation of precise circuit wiring by focusing on callosal projection neurons (CPN), which link cortical hemispheres via the corpus callosum. CPN are centrally involved in associative and cognitive function, and are often disrupted in people with autism spectrum disorders (ASD) and intellectual disabilities (ID). We identify dysregulated subcellular CPN GC proteomes after CPN-specific deletion of , a transcription factor (TF) with variants that cause ASD/ID in humans, and validate localization of dysregulated proteins to CPN GCs . We identify that disruption of Lrrtm2 - a canonically postsynaptic transmembrane protein - in CPN GCs specifically induces innervation of the amygdala, an evolutionarily ancient regulator of social behavior, cognition, and anxiety that is abnormally activated in humans with ASD. Mechanistically, we identify that deletion of from CPN disrupts targeting of Lrrtm2 to CPN GC membranes, causing cytoplasmic sequestration of key CPN GC surface proteins, and resulting in aberrant innervation of basolateral amygdala (BLA), which is typically targeted by evolutionarily older archicortex. Together, this work connects deletion of a causal ASD/ID TF, dysregulation of a non-canonical control over GC surface protein remodeling, and formation of a , subtype-specific circuit between cerebral cortex and BLA - similar mechanisms likely generalize across neuron subtypes. These results expand conceptual understanding of how diverse circuits are precisely constructed and potentially evolve, and how coordinated dysregulation of GC molecules can disrupt precise subtype-specific circuitry, contributing to diverse neurodevelopmental and neuropsychiatric disorders. - Source: PubMed
Publication date: 2026/04/12
Tillman Dustin EDurak OmerVeeraraghavan PriyaFroberg John EWheeler GarrettBudnik BogdanMacklis Jeffrey D - Myopia, particularly pathological myopia (PM), poses a significant global health burden due to its increasing prevalence and associated vision-threatening complications. Despite extensive genetic research, the molecular mechanisms underlying myopia progression remain unclear. This study aims to identify key causal proteins and metabolic pathways in myopia and PM and explore potential therapeutic targets. - Source: PubMed
Publication date: 2026/01/08
Hui JingwenCui XuehaoHan Quanhong - - Source: PubMed
Publication date: 2025/07/12
Ko JaewonFuccillo Marc VMalenka Robert CSüdhof Thomas C - Heart failure (HF) is a complex clinical syndrome with high morbidity and mortality, significantly burdening healthcare systems worldwide. Despite advances in therapy, effective treatment options remain limited. Sodium-glucose cotransporter 2 (SGLT2) inhibitors, initially developed for diabetes management, have demonstrated cardiovascular benefits, including reductions in HF hospitalizations and mortality. This systematic review examines the genomic effects of SGLT2 inhibitors in HF patients, focusing on gene expression, inflammatory biomarkers, and potential personalized treatment pathways. - Source: PubMed
Publication date: 2025/05/30
Saravana Kumar PavitraaChidambaram YogapriyaShree Devi GVenkatesan VettriselviSankaran RameshSenguttuvan Nagendra BoopathySadagopan ThanikachalamPrabhakaran Dorairaj - The cell adhesion molecule leucine-rich repeat transmembrane neuronal protein 2 (LRRTM2) is crucial for synapse development and function. However, our understanding of its endogenous trafficking has been limited due to difficulties in manipulating its coding sequence (CDS) using standard genome editing techniques. Instead, we replaced the entire LRRTM2 CDS by adapting a two-guide CRISPR knock-in method, enabling complete control of LRRTM2. In primary rat hippocampal cultures dissociated from embryos of both sexes, N-terminally tagged, endogenous LRRTM2 was found in 80% of synapses, and synaptic LRRTM2 content correlated with PSD-95 and AMPAR levels. LRRTM2 was also enriched with AMPARs outside synapses, demonstrating the sensitivity of this method to detect relevant new biology. Finally, we leveraged total genomic control to increase the synaptic levels of LRRTM2 via simultaneous mutation of its C-terminal domain, which did not correspondingly increase AMPAR enrichment. The coding region of thousands of genes span lengths suitable for whole-CDS replacement, suggesting this simple approach will enable straightforward structure-function analysis in neurons. - Source: PubMed
Publication date: 2025/02/12
Pollitt Stephanie LLevy Aaron DAnderson Michael CBlanpied Thomas A