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Possible Answers: SON, SEED, GET, ISSUE, SONS, SEEDS, SCION, SPAWN, CHILD, YOUNG, BROOD, SCIONS, CHILDREN, PROGENY, DESCENDANT, PROGENIES.
Last seen on: –USA Today Crossword – Sep 29 2022
–L.A. Times Daily Crossword – Feb 13 2022
–USA Today Crossword – Sep 28 2020
–Universal Crossword – Apr 12 2020
–Irish Times Simplex – Sep 4 2019
–Irish Times Simplex – Aug 12 2019
–The Sun – Two Speed Crossword – Jul 16 2019
–Wall Street Journal Crossword – June 19 2019 – Upfront
–The Sun – Two Speed Crossword – Jan 11 2019
-Eugene Sheffer – King Feature Syndicate Crossword – May 25 2018
-Irish Times Simplex Crossword – Nov 15 2017
Random information on the term “SON”:
6651
20658
ENSG00000159140
ENSMUSG00000022961
P18583
Q9QX47
NM_138927
NM_019973
NM_178880
NP_001278340
NP_001278341
NP_115571
NP_620305
NP_849211.3
NP_064357
NP_849211
SON protein is a protein that in humans is encoded by the SON gene.
SON is the name that has been given to a large Ser/Arg (SR)-related protein, which is a splicing co-factor that contributes to an efficient splicing within cell cycle progression. It is also known as BASS1 (Bax antagonist selected in saccharomyces 1) or NRE-binding protein (Negative regulatory element-binding protein). The most common gene name of this splicing protein- which is only found in Humans (Homo sapiens)- is SON, but C21orf50, DBP5, KIAA1019 and NREBP can also be used as synonyms.
The protein encoded by SON gene binds to a specific DNA sequence upstream of the upstream regulatory sequence of the core promoter and second enhancer of human hepatitis B virus (HBV). Through this binding, it represses HBV core promoter activity, transcription of HBV genes, and production of HBV virions. The protein shows sequence similarities with other DNA-binding structural proteins such as gallin, oncoproteins of the MYC family, and the oncoprotein MOS. It may also be involved in protecting cells from apoptosis and in pre-mRNA splicing.
Random information on the term “SEED”:
Attacks have been published that are computationally faster than a full brute force attack, though none as of 2013 are computationally feasible.
The Advanced Encryption Standard (AES), also known by its original name Rijndael (Dutch pronunciation: [ˈrɛindaːl]), is a specification for the encryption of electronic data established by the U.S. National Institute of Standards and Technology (NIST) in 2001.
AES is a subset of the Rijndael cipher developed by two Belgian cryptographers, Vincent Rijmen and Joan Daemen, who submitted a proposal to NIST during the AES selection process. Rijndael is a family of ciphers with different key and block sizes.
For AES, NIST selected three members of the Rijndael family, each with a block size of 128 bits, but three different key lengths: 128, 192 and 256 bits.
AES has been adopted by the U.S. government and is now used worldwide. It supersedes the Data Encryption Standard (DES), which was published in 1977. The algorithm described by AES is a symmetric-key algorithm, meaning the same key is used for both encrypting and decrypting the data.
Random information on the term “GET”:
The get of an animal are the offspring of a particular individual male animal. It is derived from the term “begat”, meaning to father offspring. The term is frequently used in livestock raising and informal animal husbandry, notably horse breeding to describe the offspring of a stallion. In show competition, a “get of sire” class evaluates a group of animals who have the same sire and evaluates the consistency with which a given sire is able to pass on desirable characteristics to his offspring.
Random information on the term “SEEDS”:
Non-profit organisations based in India, which may or may not be Non-governmental organisations, Indian NGOs.
This category has the following 4 subcategories, out of 4 total.
The following 200 pages are in this category, out of 204 total. This list may not reflect recent changes (learn more).
Random information on the term “SPAWN”:
Got Mercury? is a public awareness campaign about mercury levels in seafood. It is sponsored by the Sea Turtle Restoration Project (STRP) and its parent organization, the Turtle Island Restoration Network (TIRN). The name of the campaign is a snowclone of the successful Got Milk? advertising campaign.
Although the STRP was founded to protect sea turtles in their natural habitats, the organization began the Got Mercury? campaign in 2002. The campaign advocates that supermarkets and restaurants post warning signs about mercury contamination in seafood, require them to regularly screen seafood for levels of mercury under one part per million and that species that contain the “highest levels of mercury” should be removed from the shelves. In 2004, the organization created an online mercury seafood calculator, one that was mimicked by the free market Center for Consumer Freedom not long thereafter.
On March 17, 2008, Got Mercury? issued a report entitled, Mercury in Seafood: No Fair Warning, which included these findings:
Random information on the term “CHILD”:
Congenital hemidysplasia with ichthyosiform erythroderma and limb defects (also known as “CHILD syndrome”) is a genetic disorder with onset at birth seen almost exclusively in females.:485 The disorder is related to CPDX2, and also has skin and skeletal abnormalities, distinguished by a sharp midline demarcation of the ichthyosis with minimal linear or segmental contralateral involvement.:501
The acronym was introduced in 1980.
The acronym CHILD stands for the symptoms of the syndrome:
CHILD syndrome is inherited in an X-linked dominant fashion and is associated with a mutation of the NSDHL gene. This gene encodes for the enzyme 3beta-hydroxy sterol dehydrogenase which catalyzes a step in the cholesterol biosynthetic pathway. Locations of this enzyme include the membranes of the endoplasmic reticulum and on the surface of intracellular lipid storage droplets. A shortage of the enzyme may allow potentially toxic byproducts of cholesterol production to accumulate in the body’s tissues. Mutations of the gene have been reported in all three types: missense, nonsense, and stop mutations, all resulting in loss of function of NSDHL. The type of mutation is not believed to be the underlining reason for clinical variations in the extent of involvement but rather the differences in the pattern of X inactivation. Although researchers suspect that low levels of cholesterol and/or an accumulation of other substances are responsible for disrupting the growth and development of many body parts, the precise rationale for the laterality of the syndrome has yet to be determined.