SER

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Product information

Uses of L-serine

一,Physiological functions and health effects

1. Protein Synthesis and Tissue Repair：As a building block of protein, serine is involved in muscle repair, wound healing, and collagen production, and is crucial for skin elasticity and bone health.

2.‌ Neural and cognitive function：As a precursor of glycine and D-serine, serine modulates NMDA receptor activity, potentially improving memory and alleviating Alzheimer's disease symptoms.

3.Immunomodulation: Promotes antibody and immunoglobulin production, enhances macrophage activity, and improves defenses during recovery from infection or after vaccination.

4. Metabolism and Detoxification：It participates in one-carbon metabolism (such as the folate cycle), affects homocysteine ​​levels, and may reduce the risk of cardiovascular disease. It also assists in the synthesis of glutathione in the liver and eliminates free radicals and heavy metal toxins.

二,Skin care applications

1. Moisturizing and Repairing: Its small molecule properties allow it to be easily absorbed by the skin, locking in moisture, stimulating collagen production, and improving dry and damaged skin.

2. Antioxidant and anti-aging effects: By scavenging free radicals and reducing UV damage, it delays the formation of wrinkles and spots, and inhibits skin aging.

To date, five SPTLC1 mutations (C133W, C133Y, V144D, S331F, and A352V) have been

clearly associated with HSAN1 (6-8). A common feature of all HSAN1 mutants is a decrease

in in vitro enzyme activity, which is measured by the incorporation of labeled L-serine .

In addition to the reduced reactivity towards the typical substrate L-serine, the mutated

SPT appears to have a significantly increased reactivity towards the alternative substrates
L-alanine and (at least partially) L-glycine. 

This leads to the formation of a class of atypical deoxysphingolipids (dSLs), deoxysphingosine

(doxSA) when SPT uses alanine, and deoxymethylsphingosine (doxmethSA) when using

glycine. Similar to conventional sphingolipids, dSLs are also N-acetylated and are finally

converted into the deoxysphingosine (doxSO) backbone by introducing a C4-5 double

bond.

However, since SER dSLs lack the C1 hydroxyl group of ceramide, they will not be converted

into complex sphingolipids (such as sphingophospholipids or glycosphingolipids), nor can

they be degraded through the classical degradation pathway, because this pathway requires

the formation of the degradation intermediate sphingosine-1-phosphate.

SER has been found that the levels of dSLs are significantly increased not only in cells

expressing the mutated SPT, but also in the plasma of HSAN1 patients and in mice carrying

the transgenic SPTLC1 expressing the mutation. These observations support the

hypothesis that the altered substrate selectivity of the mutated SPT is the basis of the

pathophysiology of HSAN1.

The de novo synthesis of sphingolipids begins with the condensation reaction of an

activated fatty acid (usually palmitoyl-CoA) and L-serine to generate sphingosine (SA).

This reaction is catalyzed by serine palmitoyltransferase (SPT). In hereditary sensory

and autonomic neuropathy type 1 (HSAN1), SPT shows a shift in substrate specificity

towards alanine, leading to the formation of a class of atypical deoxysphingolipids (dSLs).

For sphingosine (SA) and deoxysphingosine (doxSA, 1-deoxysphingosine), the number

of hydroxyl groups is denoted by m (mono-) and d (di-), followed by the number of carbon

atoms; the second number indicates the number of double bonds.